Effects of VP on the mammalian CD. This takes place most intensely but not exclusively in the cortical and outer medullary CD. Prostaglandins PGs produced upon V1a stimulation probably luminal reduce cAMP accumulation in the cell by stimulating specific phosphodiesterases, and thus blunt all V2-dependent actions. First, VP increases the permeability of the CNT and CD to water, an effect depending on the insertion, in the luminal membrane of the cells, of preformed vesicles containing aquaporin 2 AQP2. The basolateral membrane of these cells is not a limiting factor for water permeability of the CD because it constitutively expresses other aquaporins.
Third, VP stimulates sodium reabsorption in most of the CD except in the portion located in the inner stripe of outer medulla and in the upper IM. The three combined actions of VP on the CD all contribute to increase U osm in different and complementary ways, provided prior accumulation of solutes in the medulla has been achieved via countercurrent multiplication mainly originating from the osmotic work of the thick ascending limbs in order to generate an osmotic driving force for water.
Water reabsorption progressively concentrates the luminal fluid in the CD. Because permeability of the CD to urea is relatively low, urea gets concentrated by this water removal until it reaches the tip of the papilla where VP increases urea permeability. This allows concentrated urea to diffuse into the medullary interestitium.
This intra-renal urea recycling process increases the flow of urea in the loops of Henle where urea enters through the urea transporter UT-A2  and enhances the ratio of urea concentration in urine relative to plasma in proportion to the rise in urine concentration. However, it also results in a lower efficiency of urea excretion i. Finally, stimulation of sodium reabsorption by VP should induce a relative dilution of the luminal fluid with respect to the surrounding environment, but this does not occur because water will follow isoosmotically sodium in the water permeable CD.
Thus, this effect on sodium transport will lead to an additional water reabsorption, concentrating all solutes but sodium in the CD lumen [32,76]. Besides these three V2R-mediated actions concurring to improve urine concentration, VP exhibits V1aR-mediated actions which tend to limit the V2 effects. V1aR are probably located in the luminal face of the cells [79—81]. Other studies have shown that V1a stimulation in CD activates prostaglandin synthesis which in turn reduce the V2R-dependent stimulation of adenylyl cyclase, thus reducing the intensity of V2R-mediated cellular effects [82,83] Fig.
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However, we hypothesize that this V1a—V2 antagonism should also occur in the rat, and that some unidentified factor s may have impeded their disclosure in this species, because, in several experiments, we observed larger changes in various parameters related to the urinary concentrating mechanism when dDAVP V2 stimulation only than when VP was infused V1 and V2 stimulation or than when endogenous VP was increased by dehydration [38,84,85]. Similar results have also been observed in isolated or in situ rat kidney [88,29].
The reason why V1aR-mediated effects partially blunt the antidiuretic action of VP may be to prevent excessive antidiuresis when VP secretion rises to relatively high values .
- Central vasopressin: dendritic and axonal secretion and renal actions.
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Are the levels of vasopressin required to elicit the different actions of VP on the CD the same, or are the different actions recruited successively and in which order with progressively rising levels of VP? In vivo, extremely low infusion rates of VP have been shown to reduce urine flow-rate in water diuretic humans and rats Fig.
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This suggests that the effect on water permeability is very rapid and occurs for very low concentrations of VP. The effect on urea permeability is possibly also elicited for low VP concentrations, but the resulting increase in U osm will take more time to become apparent in vivo because urea accumulation in the renal medulla is a slow process, due to significant escape of urea through venous medullary blood note that this escape is minimized in some species by unique anatomical adaptations [93—95].
In vitro, the effects of VP on water permeability of the CD and on the density of membrane particle clusters in the luminal membrane of CD cells which are now known to represent AQP2-rich vesicles are dose-dependent, as elegantly demonstrated by Harmanci et al. Star et al. Note however that, for technical reasons, this study explored urea movements in the terminal CD in an unphysiological direction from bath to lumen, i.
Because V1Rs seem to be located luminally see above , these different sensitivity are in good agreement with the fact that VP is much more concentrated in urine than in circulating blood see above. With respect to the V2R-mediated effect of VP on sodium reabsorption, although no study has directly addressed this point, we postulate that it probably requires a significantly higher VP concentration than does the effect on water permeability as for sodium transport in the thick ascending limb, see below.
This different sensitivity of VP-dependent water and sodium transport in CD is apparent when reinvestigating the data of Hawk et al. Moreover, this different sensitivity is also suggested by the fact that effects of very low infusion rates of VP to water-diuretic subjects in vivo reduces only urine flow-rate whereas larger infusion rates still within physiological limits reduce both urine flow-rate and sodium excretion . Bankir and J. Dose-dependent influence of VP on water permeability and on solute transport.
A Influence of increasing concentrations of peritubular VP on water permeability open symbols and sodium reabsorption black symbols in isolated perfused rat cortical collecting duct in vitro study. Figure drawn from original data published in  personal communication of J. Each point is the mean of four rats studied for each VP infusion rate. Redrawn and adapted from . In both cases, the water permeability response was more sensitive to low VP levels than the solute transport response. The maximum effect on water permeability was reached for VP concentrations or rates of infusion that elicited only a fraction of the maximum effect on solute transport.
A recent study suggests that it could also be activated by luminal V1aR . After the discovery of a VP-sensitive adenylate cyclase activity in the rabbit and rat thick ascending limb TAL of Henle's loop by Morel  , a number of studies have been devoted to various aspects of vasopressin action on this nephron segment .
The expected consequence of this effect is a more efficient accumulation of NaCl in the medulla by countercurrent multiplication, and thus a better driving force for water reabsorption in CD. Glucagon, calcitonin, and parathyroid hormone do indeed improve urine concentrating activity in vivo [—]. However, in the case of vasopressin, its effect on the TAL seems unimportant for the following reasons.
It is absent in the human kidney and weak in the rabbit species with relatively poor concentrating ability , significant in the rat, and strongest in the mouse and hamster species with relatively high concentrating ability. Accordingly, this effect is regarded as an adaptation related to the improvement in urinary concentrating ability and is probably restricted to rodents . This effect of VP is also very intense in vivo, as shown by the unusually high fractional excretion of these two ions in Brattleboro rats, and its dramatic reduction by chronic dDAVP treatment .
This VP effect on divalent cations is not assumed to improve the urinary concentrating mechanism. However, because the salts of these cations have a relatively low solubility, a reduction in their abundance, as urine gets more concentrated under the influence of VP, will reduce the risk of stone formation and thus will prevent a potential adverse effect of VP. This effect of VP makes sense because a low blood flow in the medulla should minimize the escape of solutes from the medullary interstitium via ascending vasa recta, thus favoring the maintenance of a high osmotic pressure which is crucial for inducing water reabsorption from the CD.
However, the renal medulla contains several different zones which not only contain different nephron segments but also exhibit with very different vascular architecture and pattern of blood supply [93—95]. Recent studies have shown that the reduction of blood flow seen after physiological elevation in P VP is restricted to the inner medulla IM , and that blood flow in the outer medulla OM is not reduced by VP .
A reduction of blood flow would be counterproductive in this area in which oxygen supply is not overdimensioned as it is in the cortex  , given the intense metabolic activity of the TALs, related to their active sodium reabsorption, a crucial step in the concentrating process .
That VP is able to selectively decrease blood flow to IM without affecting that in OM is probably due to the combination of two features. First, a direct V1aR-mediated vasoconstriction probably occurs selectively or predominantly in the most central vasa recta of the vascular bundles, equipped with a thicker layer of muscle cells than more peripheral vasa recta, and extending down to the deepest regions of the medulla .
Central vasopressin: dendritic and axonal secretion and renal actions
Second, stimulation of V2R presumably in CD because no V2R has been found in intrarenal vessels  results in the release of nitric oxide which attenuates the vasoconstrictor effects mediated by vascular V1aR . Prostaglandins have also been shown to modulate the effects of VP on IM blood flow [82,83]. Indomethacin administration results in a significant increase in medullary blood flow both in vivo and in vitro, and more so in females which have a more intense renal prostaglandin production than in males .
In addition to its effects on the kidney, it is worth mentioning that VP stimulates urea synthesis, together with glucoeogeneis, in the liver as do glucagon and epinephrine , an effect mediated through V1aR see review in [70,]. This could contribute to providing more urea to the kidney for improving urinary concentrating capacity. This interpretation is supported by the fact that V1aR in the liver are much less abundant in humans and rabbits than in rats, and absent in sheep, a pattern that parallels the degree of adaptation to water conservation in these species see review in .
The rat and human fetal and adult lung possesses V2 receptors  , most probably co-localized with ENaC in type II pneumocytes. VP has been shown to play a major role in the clearance of alveolar fluid after birth [,]. In addition, recent studies suggest that VP upregulates ENaC in the lung, as it does in the kidney . VP has been shown to be antipyretic, i.
However, no data is available regarding a possible influence of VP on body temperature in normal conditions. No study, to our knowledge, has seeked for a possible elevation in body temperature in Brattleboro rats, lacking VP, but indirect arguments suggest that it might be the case, as discussed by Bardoux et al.
Because water loss through the respiratory tract depends on the temperature difference between alveoli and outside air, a VP-dependent reduction in body temperature could contribute, although modestly, to further limit water losses through airways. Data from  and from N. Bouby and L. Bankir, unpublished observation. Data from . In both experiments, extrarenal water losses varied in parallel with urine flow-rate, suggesting that VP influences water reabsorption not only in the kidney but also in non-renal tissues probably the respiratory tract.
When urine is hyperosmotic to plasma, C H 2 O is negative. The capacity of the kidney to dilute urine appeared in lower vertebrates and was crucial for conserving solutes in species living in fresh water such as amphibians. ADH vasotocin in lower vertebrates and VP in mammals increases the permeability to water of the terminal part of the excretory organs bladder in lower vertebrates and CD in mammals and thus enables water to be reabsorbed when a favorable osmotic driving force exists.
In mammals, urine can be re-equilibrated with P osm in nephron segments located in the cortex and expressing AQP2 and V2R , i. Only when urine flows in the medulla, in which solutes have been accumulated to generate a hyperosmotic environment, can additional water be reabsorbed and lead to production of hyperosmotic urine.
Dilution and re-equilibration taking place in the cortex and concentration taking place in the medulla are always successive steps in the formation of a concentrated urine. Dilution can occur without subsequent concentration, but concentration never occurs without prior dilution. This dilution can be observed only in the absence of ADH, when the reabsorbed solutes cannot drive an equivalent flow of water because of the too low basal water permeability of these nephron segments.
When ADH is present, this active solute reabsorption in post-TAL segments will drive additional isoosmotic amounts of water. As illustrated in Table 2 and explained below, a large fraction of the VP-dependent water reabsorption occurs in the renal cortex and lesser amounts of water are further reabsorbed in the medulla. This situation is functionally appropriate for improving the efficiency of the urinary concentrating process because it limits the transit of water in the medulla and thus the risk of dissipation of the cortico—papillary osmotic gradient.
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