Galactogogues – Boosting Your Milk Supply and Production
If the clearance of a substance is greater than the inulin clearance, then clearly this substance is being added to the urine as it flows along the tubules; in other words, it is being secreted. Perhaps you have seen an illustration of a place that you felt extremely familiar with, such as a painting by Maxfield Parrish or have met someone that you immediately resonated with effortlessly at a very deep level, keep these impressions of place and personality in mind and cultivate them for they will help you construct the concept of your very own Extraphysical Homeground , Campo Spiritual, or Place of Eternal Origin. Her urine is collected in a period and the excretion flux of PAH is measured to mg each min. They looked at me. Let us consider the situation with a hyperosmotic medullary gradient and ADH present, so a concentrated urine is produced. The name METAtonin is an attempt to differentiate these two: Trachea Tracheal rings Annular ligaments Carina.
Chapter 25: Renal Physiology and Disease
The efficacy of this cleaning process is directly proportional to the excretion rate for the substance and inversely proportional to its plasma concentration Eq.
Clearance is the ratio between excretion rate and plasma concentration for the substance. Renal clearance can also be thought of as the volume of arterial plasma completely cleared of the substance in the kidneys within one min, or the number of ml arterial plasma containing the same amount of substance as contained in the urine flow per minute Eq. The glomerular filtration rate, GFR, is the volume of glomerular filtrate produced per min.
In healthy adults the GFR is remarkably constant about l each day or ml per min due to intrarenal control mechanisms.
In many diseases the renal bloodflow, RBF, and GFR will fall, whereby the ability to eliminate waste products and to regulate body fluid volume and composition will decline. The degree of impaired renal function is shown by the measured GFR. GFR is routinely measured as the endogenous creatinine clearance. The endogenous creatinine production is from the creatine metabolism in muscles and proportional to the muscle mass.
In a kg person creatinine is produced at a constant rate of 1. This production is remarkably constant from day to day, only slightly affected by a normal protein intake, and equal to the rate of creatinine excretion.
Both the serum creatinine and the renal creatinine excretion fluctuate throughout the day. Therefore, it is necessary to collect the urine for hours and measure the creatinine excretion rate ie, the urine flow rate multiplied by the creatinine concentration in the urine.
A single venous blood sample analysed for creatinine in plasma is all that is needed to provide the endogenous creatinine clearance Eq. Theoretically, two small errors disturb the picture, but both are overestimates. Most laboratories measure creatinine in serum instead of plasma, which results in an overestimation of plasma creatinine. Thus, calculation of a fraction with both an overestimated nominator and denominator results in a value close to that of GFR in almost all situations, where the renal function is near normal.
With progressive renal failure the plasma creatinine rises, and the creatinine secretion increases the nominator in the clearance expression even more, so the measured clearance will overestimate GFR. Still, the clearance provides a fair clinical estimate of the renal filtration capacity GFR. In most cases a normal creatinine clearance above 70 ml plasma per min at any age is comparable with the normal range for serum creatinine around 0.
The serum creatinine concentration is inversely proportional to the creatinine clearance, and also a good estimate of GFR. Renal failure is almost always irreversible, when the serum creatinine is above 0. Creatinine clearance versus serum creatinine. Serum [creatinine] and serum [urea] depend upon both protein turnover and kidney function.
The serum [creatinine] and [urea] are large after intake of meals extremely rich in fried meat, although the kidney function is normal false positive concentrations in Fig. Long-term hospitalisation often leads to muscular atrophy, which reduces creatinine production and excretion.
The serum creatinine concentration is maintained normal because of a similar fall in kidney function GFR. Half the osmolality of normal urine is due to urea, and the other half is mainly due to NaCl.
The osmolarity of urine varies tremendously from 50 to mOsmol per l. Physiological changes of the renal bloodflow often parallel changes of GFR. When kidneys are perfused by anoxic blood the tubular reabsorption is blocked first, and then the GFR is reduced.
The size of GFR is determined by the factors shown in Fig. The resistance of the gl omerular barrier is extremely small in healthy human kidneys. Inulin is the ideal indicator for determination of GFR, because of the following three relations: Inulin is a polyfructose from Jewish artichokes without effect on GFR.
Inulin has a spherical configuration and a molecular weight of Inulin filters freely through the glomerular barrier. Inulin is uncharged and not bound to proteins in plasma.
Inulin crosses freely most capillaries and yet does not traverse the cell membrane distribution volume is ECV. Since one litre of plasma contains around 0. In other words, they are neither reabsorbed nor secreted in the tubules. Inulin is an exogenous substance - not synthesised or broken down in the body.
Inulin is non-toxic and easy to measure. Thus, under steady-state conditions, the rate of inulin leaving the Bowman's capsulesmust be exactly equal to the rate of inulin arriving in the final urine. The main idea is to measure the amount of inulin excreted in the urine during a timeperiod were the plasma [inulin] is maintained constant by constant infusion of inulin. All inulin molecules remain in the preurine until the subject urinates.
Thus, the amountexcreted is equal to the amount filtered and Eq. The normal values for both sexes decrease with age to 70 ml per min after the age of Inulin clearance is a precise experimental measure and the ideal standard, but inulin must be infused intravenously, and the method is not necessary in clinical routine. If the clearance of a substance has the same value as the inulin clearance for the person, then the substance is only subject to ultrafiltration. Theoretically, reabsorption might balance tubular secretion and give the same result.
If the clearance of a substance is greater than the inulin clearance, then clearly this substance is being added to the urine as it flows along the tubules; in other words, it is being secreted.
Similarly, if the clearance of a substance is less than the inulin clearance, it means that the substance is being reabsorbed at a higher rate than any possible secretion.
The extracellular fluid volume ECV can be measured with inulin as inulin does not pass the cell membrane see Chapter 24 and Eq. The elimination of inulin is exponential - ie, the fraction k of the remaining amount in the body that disappears per time unit is constant see Chapter 1. Since the filtration family of substances is eliminated from the blood solely by filtration, the elimination depends only on GFR, and the distribution volume is that of inulin ECV.
All substances treated by the kidneys can be divided into three groups or families, namely the filtration-, the reabsorption-, and the secretion- family. The kidney treats the filtration family of substances see later just like inulin.
The clearance is the slope of the curve, and it is obviously a constant value that is independent of C p. The straight line shows a direct relationship between the filtration rate and the concentration for the inulin family of substances in plasma.
The reabsorption or glucose family contains many vital substances see later. For the reabsorption family of compounds, the excretion flux is equal to the filtration flux minus the reabsorption flux. The maximal reabsorption flux T max is reached above a certain threshold. Excretion rate curves for inulin can be changed into clearance by a simple mathematical procedure: Differentiating the excretion flux curve for the inulin family with respect to C p produce the renal plasma clearance curves for these substances.
Let us assume that the curves are from a resting person in steady state with a normal inulin clearance the slope of the line in Fig. For all substances belonging to the inulin family the excretion flux curves are linear, so the rate of change which is the clearance must be constant in a given condition Fig.
The results of the three excretion fluxes are plotted with C p as the dependent variable x-axis of Fig. For the reabsorption family, the clearance is zero at first, because the excretion is zero Fig. The clearance increases, and finally it approaches the inulin clearance. Therefore, the clearance is steadily increasing towards inulin clearance with increasing C p. For the secretion family, the clearance must also be equal to the excretion flux divided by C p.
When the [PAH] increases, more and more PAH is eliminated by filtration, and the secretory elimination is relatively suppressed so-called auto-suppression. The clearance for the secretion family is falling with increasing C p , and approaches that of inulin Fig. Ultrafiltation and the inulin family. The pressures governing the glomerular ultrafiltration rate GFR are called the Starling forces see equation in Fig. Normally, filtration continues throughout the entire length of the glomerular capillaries in humans, because the net ultrafiltration pressure P net is positive also at the efferent arteriole.
The average values for determinants of GFR are given in the first equation of Fig. The hydrostatic pressure gradient is an important determinant of GFR. The glomerular filtration coefficient is called K f. Vasoactive substances constrict or dilatate the glomerular mesangial cells and change the value of K f.
In other conditions, the forces opposing filtration become equal to the forces favouring filtration at some point along the glomerular capillaries.
This is called filtration equilibrium. This pressure is almost equal to the proximal tubule pressure, since there is no measurable pressure fall along this segment. Net ultrafiltration pressures in afferent and efferent end of glomerular capillaries. The Starling forces determine the final ultrafiltration pressure P net across the glomerular barrier. There is almost no colloid-osmotic pressure in Bowmans space, but an oncotic pressure of approximately 25 mmHg in the incoming plasma, mainly due to proteins, which are up-concentrated, when fluid leaves the the plasma for Bowmans space.
Hereby, the protein-oncotic pressure p gc may increase from 25 to 35 mmHg at the end of the glomerular capillary Fig. The higher the renal plasma flow RPF , the lower is the rise in p gc. A combined increase in both the afferent and the efferent arteriolar resistance as caused by most vasoconstrictors may also reduce RPF more than GFR, and increase the filtration fraction.
The net ultrafiltration pressure P net varies from 20 to 5 mmHg through the glomerular capillaries, and provides the force for ultrafiltration of a fat- and protein- free fluid across the glomerular barrier into Bowmans space and flow through the renal tubules Fig.
The ultrafiltrate is isosmolar with plasma, almost protein free, and contains low molecular substances in almost the same concentration as in plasma water. The proximal tubular reabsorption takes place through para- and trans-cellular pathways. In the peritubular capillaries, the Starling forces are seemingly adequate for capillary uptake of interstitial fluid Fig. The hydrostatic net pressure in the proximal tubules — and with it the GFR - is remarkably well maintained in spite of changes in proximal reabsorption of salt and water.
The resistance of the glomerular barrier is calculated in Fig. Normally, there is hardly any hydrodynamic resistance to glomerular ultrafiltration. Tubular reabsorption and the glucose family. T max is the maximum transfer or net reabsorption flux J reabs for glucose mol. For the reabsorption family of substances, the excretion is zero at first since the entire filtered load is reabsorbed all glucose is reabsorbed, see Fig.
The excretion flux increases then linearly with increasing filtration flux. Renal Glucose rates as a function of the plasma concentration C p. The appearance threshold is the blood plasma [glucose] at which the glucose can be first detected in the urine normally 8. This occurs when most but not all nephrons are saturated Fig.
The actual saturation threshold, the point where all nephrons are glucose-saturated, is much higher normally above The concentration difference The reabsorption capacity for glucose in the proximal tubule cells becomes saturated at these high blood concentrations Fig. The water reabsorption in the proximal tubules increases the urea concentration in the fluid. Since urea is uncharged and diffuses easily, it will diffuse passively to the peritubular capillary blood.
The passage fraction at the outlet of the proximal tubule is around 0. Urea is thus reabsorbed in the proximal tubules and also in the inner medullary collecting ducts and secreted in the thin descending and ascending limb of the Henle loop see later.
The kidney reuses urea by recirculation in the intra-renal urea recycling circuit: Inner medullary collecting ducts — medullary interstitium — loop of Henle — distal tubules — collecting ducts. The normal urea concentration in plasma is 5mM, and the excretion flux for urea is proportional to this urea concentration. The tubular passage fraction for these substances at the outlet of the proximal tubule is 0.
The reabsorption of fluid is isosmotic. Almost all filtered glucose, peptides and amino acids are also reabsorbed by the proximal tubules. The Cl- reabsorption is passive. Reabsorption of water is passive as a result of the osmotic force created by the reabsorption of NaCl. The extremely high water permeability of the proximal tubule is essential for its nearly isosmotic volume reabsorption. The active reabsorption of solutes makes the fluid slightly dilute and the interstitial fluid slightly hypertonic.
If inulin and PAH molecules are present their concentration in the fluid will rise PAH also because of proximal secretion. The actively reabsorbed solutes have lower permeabilities higher reflection coefficients than NaCl. Reabsorption of NaCl in the early and the late part of the proximal tubule.
CA stands for carboanhydrase in the brush borders of the cell. This is secondary active transport showing saturation kinetics. Glucose is a typical example. The luminal membrane contains a sodium-glucose-cotransporter SGLT 2.
A genetic defect in this protein produces familial renal glucosuria — just as a genetic defect in a similar intestinal protein SGLT 1 produces glucose-galactose malabsorption. In this segment the tubular fluid contains a high concentration of Cl - and a minimum of organic molecules. Transfer of the Cl - -ion from the tubular fluid to the blood causes the tubular fluid to become positively charged relative to the blood.
The Cl - -channels are only located in the basolateral membrane, so accumulated Cl - reaches the ISF. Paracellular reabsorption of positive ions by diffusion is augmented by the positive charge of the tubular fluid Fig. Reabsorption of NaCl in the thick ascending limb of the Henle loop. This mechanism is essential for development of medullary hypertonicity by NaCl and thus for counter current mutiplication see later. Reabsorption in the distal tubule and collecting duct.
Cellular transport processes in the distal tubule and collecting duct. The late segment is composed of two cell types just as the collecting ducts. Aldosterone enters the cell from the blood and binds to an intracellular receptor to form a complex. The collecting duct contains principal and intercalated cells just as the late distal segment, but the intercalated cell disappears in the inner medullary collecting ducts. The luminal membrane of the principal cells in the collecting ducts can be regulated from nearly water-impermeable in the absence of antidiuretic hormone, ADH to water-permeable in the presence of ADH.
The hormone increases the water-permeability by insertion of water-channels called aquaporin 2. The water-channels are stored in cytoplasmic vesicles that fuse with the luminal membrane. The basolateral membrane of the principal cell contains other aquaporins and they remain water-permeable even in the absence of ADH.
Mutations in the genes for these channel proteins cause nephrogenic diabetes insipidus. Tubular secretion and the PAH family. T max is the maximum secretion rate for PAH in the tubules Fig. Normally, the T max is 0. At low PAH concentrations in the plasma Fig. The secretion flux is maximal, when the plasma-[PAH] is high enough to achieve saturation. The weak organic acids and bases mentioned above are similarly secreted into the proximal tubule, and have secretory T max -values just like PAH Fig.
In humans of average size with an average body surface area of 1. The tubular reabsorptive capacity is normally far greater than the amount delivered in the glomerular filtrate. Above a critical concentration in the ECV of about 0. Precipitation in the joints is termed gout arthritis urica , often affecting several joints.
Urate ions are accumulated in the ECV of gout patients, and often also in patients with uraemia. High doses of probenecid compete with urate for the proximal reabsorption mechanism.
Use of this drug to patients with acute gout increases the excretion of urate in the urine. The active secretion of urate ions occurs from the blood plasma to the tubular fluid by the organic acid-base secretory system , which has a low capacity for urate. Thus, the renal tubules have a capacity of both actively reabsorbing urate ions and actively secreting them.
Secretion of organic anions across the proximal tubules. Water and solute shunting by vasa recta. This bloodflow is larger than the fluid flow through the loop of Henle. Both the vasa recta and the closely located loops of Henle from juxtamedullary nephrons consists of two parallel limbs with counter-current fluid flow in the medulla.
Vasa recta are designed as a counter current bloodflow and act as water-solute shunts that protect the medullary hyperosmotic gradient.
The endothelial lining of vasa recta is highly permeable for small molecules water, urea, NaCl, oxygen and carbon dioxide. Vasa recta also serve as a nutritive source to the medulla. Vasa recta receive blood from the efferent arterioles and consequently have an elevated colloid osmotic pressure and reduced hydrostatic pressure Fig.
The net force in these vascular loops favours net fluid reabsorption. Let us consider the situation with a hyperosmotic medullary gradient and ADH present, so a concentrated urine is produced. Accordingly, this blood must gradually supply water to the hyperosmolar, interstitial fluid by passive osmosis, and passively reabsorb solutes NaCl and urea by diffusion.
Hereby, the interstitium is temporarily diluted and the blood is concentrated. In the ascending portion the blood passes regions with falling osmolarity, and the blood gradually absorbs water osmotically and delivers solutes to the interstitium by diffusion. The flow in the ascending vasa recta is larger than in the descending limb, because water from the Henle loop is also reabsorbed. Passive counter-current exchange occurs in vasa recta, with diffusion of solutes along black arrows.
Passive osmotic flux of water from the blood to the hyperosmolar interstitium occurs along stippled, blue arrows. The active counter-current multiplier in the thick ascending limb with a single effect at each horizontal level. The gross effect of the passive counter-current exchange in the vasa recta is that of a water shunt passing the medullary tissue, whereas solutes recycle and thus are maintained in medulla.
Water is shunted from limb to limb without disturbing the inner medulla. The passive counter-current exchange and low bloodflow through the vasa recta curtail the medullary hyperosmotic gradient Fig. Concentration or dilution of urine. The thin ascending limb of Henle is impermeable for water, but highly permeable for NaCl and less so for urea. The thick ascending limb is also impermeable for water and also for urea. The water permeability of the cortical and medullary collecting ducts increase with increasing concentrations of antidiuretic hormone ADH in the peritubular blood.
The ascending limb of the Henle loop is impermeable to water and actively transports NaCl from the preurine into the surrounding interstitium. Thus solute and fluid is separated and the tubular fluid becomes diluted. Energy is necessary to establish the hyperosmotic gradient. The total osmolarity in the inner medullary interstitial tissue can be as high as mOsmol per l, when the urine is maximally concentrated. The renal cortex fluid is isotonic with the plasma.
When the isotonic fluid from the proximal tubules passes down through the hypertonic medulla in the descending thin limb of the Henle loop, water moves out into the medullary interstitium by osmosis, making the tubular fluid concentrated.
This is because the epithelial cells of the thin descending limb are highly permeable to water but less so to solutes NaCl and urea. Water is reabsorbed and returned to the body via vasa recta and the renal veins. At the bend of the loop the fluid has an osmolarity equal to that of the surrounding medullary interstitial fluid. However, the tubular fluid has a greater concentration of NaCl and a smaller concentration of urea than the surroundings.
In contrast to the thin and thick ascending limb, most cell membranes including those of the proximal tubules and the thin descending limb of the Henle loop, are water-permeable under all circumstances. This is because these cell membranes contain water-channel proteins called aquaporins. As new fluid enters the descending limb of the Henle loop, the hyperosmotic fluid in the bottom of the loop is pushed into the ascending limb, where NaCl is separated from water.
The thick ascending limb is a counter-current multiplier with a high multiplication capacity. The NaCl is reabsorbed repeatedly in the thick ascending limb of the Henle loop. The passive counter-current exchange in the vasa recta and the active counter-current NaCl reabsorption in the thick ascending limb combine into a solute-water separator , when ADH is present.
Another component in the maintenance of the medullary hyperosmotic gradient is addition of urea to the tubular fluid in the thin segment of the Henle loop. Urea is then trapped in the lumen, because all nephron segments, from the thick ascending limb through the outer medullary collecting duct, are impermeable to urea. As the tubular fluid flows through the distal tubules, cortical collecting ducts and outer medullary collecting ducts, its urea concentration rises progressively, because these segments are essentially urea-impermeable whether or not ADH is present.
In the presence of ADH, water is reabsorbed but urea is not and the osmolarity of the fluid increases. The distal fluid contains much urea and less NaCl. In reverse, the inner medullary collecting duct cells have urea-transporters that are ADH-sensitive. Thus large amounts of urea are reabsorbed at low urine flows, and the inner medullary interstitial fluid is loaded with urea that diffuses back to the tubular fluid through the thin descending and ascending limb in this urea recycling process.
Without passive urea recycling, the medullary interstitial osmolarity contributed by NaCl would have to double and thus the energy demand. Without the medullary hypertonic gradient we would be unable to produce concentrated urine when water depleted.
A high osmolarity in the medullary interstitium enhances passive water reabsorption when ADH is present. ADH increases the concentration of solutes in the collecting ducts, and reduces the loss of water.
Dilution of urine large urine flow. In the absence of ADH, the distal tubules, cortical collecting ducts and outer medullary collecting ducts are impermeable to water.
The medullary collecting duct reabsorbs NaCl actively and is slightly permeable to water and urea in the absence of ADH. When ADH is absent, the fluid leaving the distal tubules remains hypotonic. A daily solute loss of mOsmol, under these conditions, implies a daily water loss of at least 14 l.
The Fick's principle mass balance principle is used to measure the renal plasma clearance at low plasma [PAH] , since at low concentrations - the blood is almost cleared by one transit. The law of mass balance states that the infusion rate of PAH is equal to its excretion rate at steady state. A methodological short cut is to measure the [PAH] in the medial cubital vein only, instead of the true arterial [PAH] by arterial catheterisation.
The ERPF principle avoids complex invasive procedures such as catheterisations. The RBF falls drastically, when the mean arterial pressure is below 9. The medullary bloodflow is always small in both absolute and relative terms. Any severe RBF reduction as in shock, easily leads to ischaemic damage of the medullary tissues resulting in papillary necrosis and ultimately to failure of renal function. During such pathophysiological conditions, prostaglandins PGE 2 and PGI 2 are secreted from the mesangial and endothelial cells due to sympathetic stimulation.
These prostaglandins dilatate the afferent and efferent glomerular arterioles and dampen the renal ischaemia caused by sympatho-adrenergic vasoconstriction. The renal autoregulation is mediated by myogenic feedback and by the macula densa-tubulo-glomerular feedback mechanism.
Myogenic feedback is an intrinsic property of the smooth muscle cells of the afferent and efferent arterioles. The myogenic response allows preglomerular arterioles to sense changes in vessel wall tension T and respond with appropriate adjustments in arteriolar tone.
Stretching of the cells by a rise in arterial transmural pressure D P elicits smooth muscle contraction in interlobular arteries and afferent arterioles Fig.
During sleep the mean arterial pressure decreases kPa, which would lower P gc and GFR without autoregulation. Autoregulation with maintained RBF and GFR means that also the filtered load and the sodium excretion is maintained during sleep and variations in daily activities.
The macula densa- TGF mechanism is described below. The predominate form in which nitrogen is excreted by birds uric acid requires little water for excretion because it isn't very soluble in water. However, it does require a significant amount of protein to maintain it in a colloidal suspension in the urine i. The source of some of this protein is the plasma, as significant amounts pass through the glomerular filtration barrier.
This protein is not lost because it is broken down when the urine enters the lower colon Goldstein et al. In the colon, the composition of the urine is altered in several ways. The urine spheres are broken down, as is the protein that aided the formation of those spheres. Much of this degradation is accomplished by bacteria. The amino acids or peptides that result are either used by the bacteria or absorbed by the epithelium of the colon Braun Casotti and Braun In birds, urine is conveyed to the cloaca, and moved by reverse peristalsis into the colon and digestive ceca.
Digestive ceca have been well studied for non-passerine birds and have been shown to absorb substrates and water. The ceca of passerine birds have been suggested to be non-functional because of their small size. Three-dimensional reconstruction of the ceca of House Sparrows Passer domesticus from serially-sectioned tissue showed that the ceca have a central channel with a large number of side channels. Electron micrographs indicated that all of the channels are lined by epithelial cells with a very dense microvillus brush border as well as a region densely packed with mitochondria just below the brush border.
It is possible that the row of mitochondria below the brush border is present to provide ATP to power substrate transport. Although the importance of small ceca for fluid homeostasis remains to be determined, these data suggest that the small ceca of passerine birds may function in fluid and electrolyte e.
Light micrograph and electron micrographs of a House Sparrow cecum. A A light micrograph of a cecum cut in sagittal section. The image shows one central channel with a proximal opening to the colon upper right of section. Side channels arrows can be seen branching from the central channel.
B Higher power light micrograph of a cecum. The image illustrates the columnar cells that line the channels bracket with their well developed brush border arrow.
C Electron micrograph of a House Sparrow cecum. The image shows a portion of the epithelial cells that line channels of the ceca. Evident is a dense microvillus brush border on the apical surface of the cells and tight junctions TJ between the cells.
Just below the brush border is a very dense layer of mitochondria bracket. Reyes and Braun As described above, the colon and ceca of birds can substantially modify the urine that initially enters the cloaca coprodeum.
As a result, the composition of bird droppings can differ dramatically from the composition of the urine and feces that initially entered the colon or large intestine Figure Depending on diet and access to water, droppings may have considerably less water, solutes sodium and potassium , and uric acid or urate than the original urine and feces Figure Of course, if a bird consumes more of these substances than needed, the composition of droppings will differ and more water, solutes, and urates can, as needed, be excreted in the droppings.
The coordinated action of the kidneys, lower GI tract, and the salt glands see below in the regulation of fluid and ion balance is a classic example of the integration of organs required to maintain homeostatic balance. No single organ appears to have an outstanding capacity to conserve ions and water, but instead they all function in concert to maintain total body fluid homeostasis to allow birds to inhabit a wide range of environments Braun Modification of urine and feces in the lower GI tract colon and ceca of birds.
Can birds be ammonotelic?? Uric acid is a relatively non-toxic nitrogen end product. It is relatively insoluble and hence excreted with little water. Uricotely, however, is costly. More energy is needed to excrete a unit of waste nitrogen as uric acid than as urea or ammonia. In contrast to uric acid, ammonia is highly soluble, cheap to synthesize, but fairly toxic.
It can only be used as a nitrogenous waste by animals with high rates of water turnover that permit almost continuous elimination, such as in aquatic animals Tsahar et al. Preest and Beuchat suggested that it might be advantageous for birds that ingest large amounts of dilute, protein-poor nectar to shift from uricotely to ammonotely. Thus, ammonia can be voided rapidly, and the costs of synthesizing urates can be reduced.
Thus, Preest and Beuchat proposed that high energy demands and high water fluxes favor ammonotely. Subsequently, Roxburgh and Pinshow found that the Palestine Sunbirds also switched from uric acid to ammonia excretion under some conditions.
However, Roxburgh and Pinshow noted that in sunbirds with high water intake, the concentration of urate was higher in the ureters the tubes that carry urine from the kidneys to the cloaca than in excreta. They argued that ammonotely in Palestine Sunbirds was only 'apparent' because it was not a result of excessive excretion of ammonia, but rather the result of a reduction in excreted urate resulting from post-renal modification of urine.
Recently, Tsahar et al. These authors, like Roxburgh and Pinshow found that protein concentration was lower in excreta than in ureteral urine, and hypothesized that some of the protein associated with urate spheres was digested in the lower intestine and recovered. Why would it be advantageous for birds to recover a nitrogenous metabolic waste? Although uric acid is considered primarily a nitrogenous waste, it also has a major function as a powerful antioxidant in both birds and mammals Tsahar et al.
So, can birds be ammonotelic? In some cases, as with Anna's Hummingbirds, ammonotely may be a response to the ingestion of lots of water facultative ammonotely. In other cases, ammonotely may simply be 'apparent', with urine produced by the kidneys being urotelic but the actual excreta being ammonotelic because of reabsorption of uric acid in the lower intestine or colon prior to defecation. Because the kidneys of birds cannot produce a hypertonic urine with lots of ions like sodium , the excretion of excess salt is a potential problem.
Even quicker than humans, birds would be severely dehydrated after drinking saltwater and ingesting salty food. However, many species of birds, especially marine birds and shorebirds, can drink seawater as their only source of water. This is possible because these birds have another way other than the kidneys to eliminate excess salt - salt glands.
Salt glands of birds likely evolved from nasal glands of reptiles, probably in the late Paleozoic. They lie immediately under the skin in supraorbital depressions of the frontal bone in the skull of Charadriiform birds, but in other groups they may be located above the palate or within the orbit of the eye. Skulls of fossil birds, Ichthyornis and Hesperornis, have similar depressions Figure 14 , suggestin g these birds lived in marine habitats. The salt glands of marine birds and some falconiform and desert birds secrete excess NaCl via the salt glands using less water than is consumed, which generates free water Hughes Hesperornis skull note depression above eye socket where salt gland would be located.
Salt glands have been reported in several avian orders Spheniciformes , Procellariformes , Charadriiformes, Pelecaniformes, Anseriformes, and Phoenicopteriformes.
Even though most studies of osmoregulation in birds have been conducted with marine taxa, nasal secretions are not to be restricted to these species. The presence of functional salt glands has been documented in several terrestrial orders. For example, Roadrunners Geococcyx californianus and Savanah Hawks Heterospizias meridionalis , have active salt glands and can produce hypertonic secretions in response to their protein-rich diets. Although these species are not stressed by high saline load, the active secretions of salt gland allows them to minimize water losses.
Other desert birds, such as the Sand Partridge Ammoperdix heyi and the Ostrich Struthio camelus , have functional salt glands that are stimulated in response to high temperature. Thus, salt glands are not restricted to birds that live in saline or maritime habitats, but are also present in some terrestrial forms that consume little water Sabat Salt glands have a system of countercurrent blood flow to remove and concentrate salt ions from the blood Figures 15 and The paired, crescent-shaped glands each contain several longitudinal lobes approximately 1 mm in diameter and each lobe contains a central duct from which radiate thousands of tubules enmeshed in blood capillaries.
These tiny capillaries carry blood along the tubules of the gland, which have walls just one cell thick and form a simple barrier between the salty fluid within the tubules and the bloodstream.
It is here that salt excretion occurs. When a bird drinks seawater, sodium enters the blood plasma from the intestine and the solute concentration of the blood plasma increases. This causes water to move out of cells osmosis , increasing the extracellular fluid volume ECFV. The increases in blood plasma solute concentration and ECFV stimulate salt gland secretion Hughes Glomerular and medullary architecture in the kidney of Anna's Hummingbird.
Journal of Morphology An overview of osmoregulation in birds. Abstract - VI International Symposium of avian endocrinology. Academy of Breastfeeding Medicine Clinical Protocol 9: Systematic Review of the Efficacy of Herbal Galactagogues. Journal of Human Lactation. Use of Herbals as Galactagogues. Journal of Pharmacy Practice April vol. Blessed Thistle and Increasing Milk supply.
Alfalfa and Increasing Milk Supply. Galactogogues — Boosting Your Milk Supply and Production Herbs and medications that increase your milk supply are known as galactagoges ga-lac-ti-gogs. Fenugreek There are many common herbal supplements available that have been shown to be effective for increasing your milk production. Blessed Thistle This plant has been used as a medicine for hundreds of years, and has been shown to increase milk supply.
Alfalfa A type of pea, alfalfa has a mild effect on increasing milk supply and is often used in combination with fenugreek. Compiled from the following References: