Effect of vasopressin on sodium excretion and plasma antinatriferic activity in the dog

Buckalew, V. M.; Dimond, KA

doi:10.1152/ajplegacy.1976.231.1.28

Cited by 27 publications

(23 citation statements)

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“…(1) In several previous studies, the AVP-induced natriuresis was assumed to result from the volume expansion induced by fluid loads given orally and/or intravenously before and/or during AVP administration. The authors proposed that this expansion induced the release of another mediator inhibiting renal tubular sodium transport 4,39 ; however, our experiments show that AVP increased sodium excretion even in the absence of any fluid load. (2) Prostaglandins are known to reduce sodium transport in the CD 40 and to increase medullary blood flow, 41,42 two effects that each will contribute in different ways to increased sodium excretion.…”

Section: V1ar Effectscontrasting

confidence: 76%

“…[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: 79%

“…Several previous studies already observed this simultaneous increase in sodium excretion and urine flow rate after AVP infusions. 4,6,8 In these experiments, it would have been difficult to evaluate the mean plasma AVP (P AVP ) level reached during 6 h (duration of the urine collection). Measurements of the AVP excretion rate provide more integrated information during this period.…”

Section: Urinary Avp Concentration In Different Experimental Conditiomentioning

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 Effectscontrasting

confidence: 76%

Section: V1ar Effectsmentioning

confidence: 79%

Section: Urinary Avp Concentration In Different Experimental Conditiomentioning

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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“…The specificity in AVP may lie in the fact that AVP, among pressor agents, has the strongest vasoconstrictor activity, 4 has a natriuretic action, 5 and enhances baroreceptor reflex activity 6 ; one or more of these actions of AVP may form the basis of the mechanism for the WAP. Because there is no evidence that these actions of AVP exist in SHR alone, one needs to postulate that SHR are more sensitive than WKY to these actions of AVP.…”

Section: Antihypertensive Effect Of Vasopressin Withdrawal In Young Amentioning

confidence: 99%

Antihypertensive effect of vasopressin withdrawal in young and adult spontaneously hypertensive rats.

Chiu

McNeill

1989

Hypertension

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The extent to which age influences the effect of prolonged intravenous infusion and withdrawal of arginine vasopressin (AVP) on blood pressure was investigated in spontaneously hypertensive rats (SHR) and their normotensive Wistar-Kyoto controls (WKY) of 6-, 10-, 14-, 18-, and 22-week age groups. The pressor response to AVP (20 ng/kg/min for 3 hours) was relatively well maintained in WKY but showed an age-dependent tachyphylaxis in SHR. After cessation of the infusion, arterial pressure of SHR fell in all age groups. In contrast, withdrawal of AVP in WKY resulted in little or no hypotensive response. Thus, a withdrawal-induced antihypertensive phenomenon (WAP) to AVP was specific to SHR. The magnitude of the WAP was significantly correlated with the level of initial blood pressure in SHR (r=-0.81,p<0.001). The magnitude of the tachyphylaxis during the AVP infusion was also correlated with the level of initial blood pressure in SHR (r=-0.66, p<0.001). Accordingly, a significant correlation was found between the magnitude of the WAP and the degree of tachyphylaxis to the pressor activity of AVP in SHR (r=0.69, p< 0.001). The significance of this is unknown, but it might mean that a common underlying mechanism existed in the expression of the tachyphylactic phenomenon and the WAP in SHR. Finally, an apparent enhancement in the baroreceptor reflex sensitivity was observed in both SHR and WKY during the infusion of AVP, but the magnitude of this enhancement appeared to be greater in SHR than in WKY. We conclude that in all age groups, a WAP to AVP is observed in SHR but not in WKY; the magnitude of the WAP appears to depend on the level of the hypertension in SHR. (Hypertension 1989;14:66-72) P reviously, 1 -2 we described a hypotensive response that occurred in spontaneously hypertensive rats (SHR) after the cessation of a prolonged intravenous infusion of a pressor dose of arginine vasopressin (AVP). This fall of arterial pressure below basal control levels did not occur in normotensive Wistar-Kyoto rats (WKY). Furthermore, the hypotensive response in SHR was of a magnitude (approximately 45-50 mm Hg) sufficient to reduce arterial pressure in these SHR to normotensive levels. Thus, a withdrawal-induced antihypertensive phenomenon (WAP) was specific to SHR. The WAP was reduced or absent when angiotensin II or phenylephrine was infused at pressor doses.1 " 3 Accordingly, the WAP appeared to be specific for AVP in SHR. The specificity in

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The Kidney and Regulation of Blood Pressure

Hall¹,

Guyton²

1992

Renovascular and Renal Parenchymatous Hypertension

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Effect of vasopressin on sodium excretion and plasma antinatriferic activity in the dog

Cited by 27 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

Antihypertensive effect of vasopressin withdrawal in young and adult spontaneously hypertensive rats.

The Kidney and Regulation of Blood Pressure

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