Natrriuresis produced by vasopressin or hemorrhage during water diuresis in the dog

Mh, Humphreys; Friedler, RM; Earley, Laurence E.

doi:10.1152/ajplegacy.1970.219.3.658

Cited by 49 publications

(31 citation statements)

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“…[2][3][4][5][6][7][8][9] The dose-response curve performed in this study shows that this effect occurred only for high doses (15 and 50 g/kg BW) that probably increased P AVP levels distinctly above those involved in water conservation, even after 24 h of water deprivation, as judged here by the urinary AVP data (Table 2). With lower doses (0.1 and 1 g/kg BW), likely corresponding to the range of usual osmotic stimuli, Figure 4.…”

Section: V1ar Effectsmentioning

confidence: 80%

“…Of note, AVP concentration is known to be higher in the CD lumen and in the medullary interstitium than in peripheral blood. 17 (3) Finally, the natriuretic effects of AVP could be due to pressure-natriuresis resulting from the vasopressor effects of the hormone, either within the whole circulation or selectively within the kidney vasculature.…”

Section: V1ar Effectsmentioning

confidence: 99%

“…In the isolated microperfused CD, V2R activation increases sodium transport, 1 an effect that should reduce sodium excretion in vivo; however, in a number of studies, AVP infusion in animals and humans has been shown to induce an increase in sodium excretion. [2][3][4][5][6][7][8][9] It is usually assumed that AVP might contribute to some forms of hypertension by its vasoconstrictive effects, but an increase in sodium excretion, if it occurred in normal life, should more likely contribute to lower BP.…”

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confidence: 99%

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Sodium Excretion in Response to Vasopressin and Selective Vasopressin Receptor Antagonists

Perucca

Bichet²,

Bardoux

et al. 2008

Journal of the American Society of Nephrology

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The mechanisms by which arginine vasopressin (AVP) exerts its antidiuretic and pressor effects, via activation of V2 and V1a receptors, respectively, are relatively well understood, but the possible associated effects on sodium handling are a matter of controversy. In this study, normal conscious Wistar rats were acutely administered various doses of AVP, dDAVP (V2 agonist), furosemide, or the following selective non-peptide receptor antagonists SR121463A (V2 antagonist) or SR49059 (V1a antagonist). Urine flow and sodium excretion rates in the next 6 h were compared with basal values obtained on the previous day, after vehicle treatment, using each rat as its own control. The rate of sodium excretion decreased with V2 agonism and increased with V2 antagonism in a dose-dependent manner. However, for comparable increases in urine flow rate, the V2 antagonist induced a natriuresis 7-fold smaller than did furosemide. Vasopressin reduced sodium excretion at 1 g/kg but increased it at doses Ͼ5 g/kg, an effect that was abolished by the V1a antagonist. Combined V2 and V1a effects of endogenous vasopressin can be predicted to vary largely according to the respective levels of vasopressin in plasma, renal medulla (acting on interstitial cells), and urine (acting on V1a luminal receptors). In the usual range of regulation, antidiuretic effects of vasopressin may be associated with variable sodium retention. Although V2 antagonists are predominantly aquaretic, their possible effects on sodium excretion should not be neglected. In view of their proposed use in several human disorders, the respective influence of selective (V2) or mixed (V1a/V2) receptor antagonists on sodium handling in humans needs reevaluation. 19: 172119: -173119: , 200819: . doi: 10.1681 The mechanisms by which arginine vasopressin (AVP) exerts its antidiuretic and its pressor effects are relatively well understood. On the one hand, AVP improves water conservation by increasing the permeability to water of the renal collecting duct (CD), an effect mediated by the V2 receptors (V2R) and permitted by the insertion in the luminal membrane of principal cells of preformed aquaporin 2 (AQP2) molecules. This allows more water to be reabsorbed when these ducts traverse the hyperosmotic medulla. On the other hand, AVP increases blood pressure (BP) by inducing a vasoconstriction through its binding to V1a receptors (V1aR) expressed in vascular smooth muscle cells. For these two different effects, in vivo studies are in good agreement with the expectations based on results obtained in vitro. J Am Soc NephrolIn contrast, the experiments intended to study the effects of AVP on sodium handling in vitro or in vivo provide results that are difficult to reconcile. In the isolated microperfused CD, V2R activation increases sodium transport, 1 an effect that should reduce sodium excretion in vivo; however, in a number of studies, AVP infusion in animals and humans

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Section: V1ar Effectsmentioning

confidence: 80%

Section: V1ar Effectsmentioning

confidence: 99%

mentioning

confidence: 99%

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Sodium Excretion in Response to Vasopressin and Selective Vasopressin Receptor Antagonists

Perucca

Bichet²,

Bardoux

et al. 2008

Journal of the American Society of Nephrology

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“…However, the effect of vasopressin on sodium excretion is less clear. A large number of studies have shown that vasopressin infusion increases sodium excretion in vivo in rats, dogs, and sheep (e.g., references [1][2][3][4]. This natriuretic effect is difficult to reconcile with the fact that, in vitro, vasopressin stimulates sodium reabsorption in the isolated perfused CD (5,6), in the amphibian bladder (a tissue that shares a number of similarities with the mammalian CD) (7), and in several cell lines issued from these two tissues (8 -10).…”

mentioning

confidence: 99%

Vasopressin-V2 Receptor Stimulation Reduces Sodium Excretion in Healthy Humans

Bankir

Fernandes

Bardoux

et al. 2005

Journal of the American Society of Nephrology

121

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In addition to its effect on water permeability, vasopressin, through its V2 receptors (AVPR2), stimulates Na reabsorption in the collecting duct by increasing the activity of the amiloride-sensitive sodium channel ENaC. This study evaluated whether dDAVP (a potent AVPR2 agonist) reduces sodium excretion in healthy humans (n ‫؍‬ 6) and in patients with central (C; n ‫؍‬ 2) or nephrogenic (N) diabetes insipidus (DI) as a result of mutations of either the aquaporin 2 gene (AQP2; n ‫؍‬ 3) or AVPR2 (n ‫؍‬ 10). dDAVP was infused intravenously (0.3 g/kg body wt in 20 min), and urine was collected for 60 min before (basal) and 150 min after the infusion. dDAVP markedly reduced both urine flow rate and sodium excretion in healthy individuals. A reduction in sodium excretion was also observed in CDI and NDI-AQP2 patients but not in NDI-AVPR2 patients. The magnitude of the fall in sodium excretion correlated with the rise in urine osmolality and the fall in urine output but not with the simultaneously observed fall in mean BP. These results suggest that the dDAVP-induced antinatriuresis is due to a direct V2 receptor-dependent stimulation of sodium reabsorption in the collecting duct and is not secondary to a hemodynamic effect. In conclusion, this study reveals a potent V2-dependent antinatriuretic effect of vasopressin in humans. The possibility that an inappropriate stimulation of ENaC by vasopressin might lead to significant sodium retention in chronic situations remains to be determined. 16: 192016: -192816: , 200516: . doi: 10.1681 I nappropriate retention of sodium and water by the kidney is thought to be a key factor in several forms of hypertension. Thus, it is important to identify factors that may favor excessive sodium reabsorption by the kidney. Vasopressin is known to promote water conservation by increasing the permeability to water of the collecting ducts (CD), thus allowing osmotically driven water reabsorption along these ducts when dilute distal tubular fluid enters them in the cortex and later when they traverse the hyperosmotic medulla. However, the effect of vasopressin on sodium excretion is less clear. A large number of studies have shown that vasopressin infusion increases sodium excretion in vivo in rats, dogs, and sheep (e.g., references 1-4). This natriuretic effect is difficult to reconcile with the fact that, in vitro, vasopressin stimulates sodium reabsorption in the isolated perfused CD (5,6), in the amphibian bladder (a tissue that shares a number of similarities with the mammalian CD) (7), and in several cell lines issued from these two tissues (8 -10). This effect on sodium reabsorption is inhibitable by amiloride and has been shown to result from activation of the endothelial sodium channel ENaC (11). Moreover, chronic elevation of vasopressin or infusion of its V2 agonist dDAVP (12) has been shown to increase the abundance of mRNA (13) and protein (14) of the ␤ and ␥ subunits of ENaC and to enhance markedly the subsequent functional response (water and sodium reabsorption) to exoge...

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“…Intracranial or systemic administration of hypertonic saline releases ADH in the dog (Verney, 1947), sheep (Blaine et al 1975;Scott & Morton, 1976), goat (Andersson, Olsson & Warner, 1967;Lishajko & Andersson, 1975) and rat (George, 1976). It has been established also that ADH is natriuretic in the dog (Humphreys, Friedler & Earley, 1970;Kurtzman, Rogers, Boonjarern & Arruda, 1975), sheep (Scott & Morton, 1976), goat (Andersson, 1955) and rat (Gershkovich, 1975). It is possible that the natriuretic effect of hypertonic saline in all these species is brought about by the ADH released as shown in sheep by Scott & Morton (1976).…”

Section: Discussionmentioning

confidence: 99%

Search for a natriuretic mechanism sensitive to sodium in the brain of the monkey.

Kumar¹,

Swaminathan²

1977

The Journal of Physiology

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SUMMARY1. The effects of hypertonic saline infusion into the third ventricle were investigated in ten monkeys which were pre-operated, trained, and used in the conscious state under controlled conditions.2. In non-hydrated monkeys, intraventricular infusion of NaCi 1-0 M, 0.01 ml./min for 30 min did not affect urine volume or Na output but produced a small increase in urine osmolality. Comparable infusion of NaCl 0-15 M had no effect on any parameter.3. In monkeys undergoing water diuresis (with i.v. infusion of 5 % dextrose), intraventricular hypertonic saline produced large reciprocal changes in urine volume and osmolality while urine Na showed no significant change. The effects on urine volume and osmolality were greater than those of lysine-vasopressin 30 m-u./kg i.v.4. The absence of natriuresis after intraventricular hypertonic saline infusion in the monkey was in notable contrast to the results reported in lower species. However, the data suggested that the infusion probably released ADH as in other species.

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Natrriuresis produced by vasopressin or hemorrhage during water diuresis in the dog

Cited by 49 publications

References 0 publications

Sodium Excretion in Response to Vasopressin and Selective Vasopressin Receptor Antagonists

Sodium Excretion in Response to Vasopressin and Selective Vasopressin Receptor Antagonists

Vasopressin-V2 Receptor Stimulation Reduces Sodium Excretion in Healthy Humans

Search for a natriuretic mechanism sensitive to sodium in the brain of the monkey.

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