Renal vascular effects of angiotensin II, arginine-vasopressin and bradykinin in rats: Interactions with prostaglandins

Hofbauer, Karl G.; Dienemann, Hendrik; Forgiarini, Peter; Stalder, R.; Wood, Jeanette M.

doi:10.1016/0306-3623(83)90086-1

Cited by 21 publications

(14 citation statements)

References 6 publications

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“…vasopressin infusion, together with a potentiation of renal vasoconstrictor response by a cyclooxygenase inhibitor (Oliver et al 1982). Potentiation of renal responses by indomethacin has also been observed in the rat (Hofbauer et al 1983;Gardiner et al 1991). However, consistent with our present results, Cooper and Malik (1984) have reported that indomethacin does not affect V 1 receptor-mediated vasoconstriction in the isolated rat kidney although the vasopressin-induced increases in PGE 2 and 6-keto-PGF 1 output are abolished concomitantly.…”

Section: Discussionsupporting

confidence: 89%

Nitric oxide, but not vasopressin V2 receptor-mediated vasodilation, modulates vasopressin-induced renal vasoconstriction in rats

Loichot

Cazaubon

Jong

et al. 2000

Naunyn-Schmiedeberg's Arch Pharmacol

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The renal vascular response to vasopressin and its modulation were evaluated in vivo by infusing the peptide directly into the renal artery of anaesthetized rats. The intra-renal artery (i.r.a) infusion of vasopressin induced a dose-dependent decrease in renal blood flow. Vasoconstriction was obvious at a dose of 3 ng/kg per min and reached a maximum at 100 ng/kg per min. The dose required for a half-maximal response (ED50) was 24+/-4 ng/kg per min (mean+/-SEM, n=8), corresponding to an estimated concentration in renal arterial blood required for a half-maximal response (EC50) of 1.9+/-0.6 nM. Thiobutabarbitone anaesthesia markedly increased plasma vasopressin concentration. This increase was prevented partially by hypotonic hydration of the rats without any change in the renal vascular response to exogenous vasopressin. Vasopressin-induced vasoconstriction dose/response curves were similar in homozygous and heterozygous Brattleboro rats. Infusion of desmopressin (1-1000 ng/kg per min, i.r.a.), a vasopressin V2 receptor-selective agonist, failed to induce renal vasodilation or vasoconstriction. In the presence of SR 49059 (1 mg/kg i.v.), a vasopressin V1A receptor antagonist that completely abolished the vasopressin-induced renal vasoconstriction, desmopressin again failed to induce vasodilation. Inhibition of nitric oxide synthase by N(omega)-nitro-L-arginine (L-NNA, 100 microg/kg for 10 min and 7.5 microg/kg per min, i.r.a.) enhanced vasopressin-induced renal vasoconstriction (EC50 0.6+/-0.1 nM, P<0.05). In contrast, cyclooxygenase blockade by indomethacin (5 mg/kg, i.v.) neither modified the vasopressin-induced decrease in renal blood flow nor altered the potentiation of vasoconstriction by L-NNA. These results show that the constrictor response of the rat renal vascular bed in vivo is observed only with high local concentrations of vasopressin. This hyporeactivity in vivo was not explained by an anaesthesia-elicited increase in endogenous vasopressin, nor by a modulatory effect linked to V2 receptor activation or prostanoid release. In contrast, NO release contributed to the attenuation of vasopressin-induced renal vasoconstriction.

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Section: Discussionsupporting

confidence: 89%

Nitric oxide, but not vasopressin V2 receptor-mediated vasodilation, modulates vasopressin-induced renal vasoconstriction in rats

Loichot

Cazaubon

Jong

et al. 2000

Naunyn-Schmiedeberg's Arch Pharmacol

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“…An uncritical reading of the published literature on the cardiovascular effects of exogenous vasopressin could give the impression that this potent vasoconstrictor neuropeptide (Gardiner et al, 1988a) does not exert pressor effects because any increase in peripheral resistance it causes is offset by a baroreflexmediated reduction in cardiac output (see Bennett & Gardiner, 1986a;Gardiner & Bennett, 1986), together with activation of vasodilator systems that may be dependent on V2-receptor-mediated mechanisms (Hofbauer et al, 1983;Walker, 1986;Liard, 1988). The present study produced results germane to these points.…”

Section: Discussionmentioning

confidence: 65%

“…It has become clear, however, that bolus doses of exogenous vasopressin may have regionally-selective effects on vascular resistances in several species, including conscious rats (Gardiner et al, 1988a) and that these may be due to indirect actions of vasopressin in the renal vascular bed (e.g. Hofbauer et al, 1983;Walker et al, 1988). Furthermore, there are indications that vasopressin may exert systemic vasodilator actions in conscious rats 1 Author for correspondence.…”

Section: Introductionmentioning

confidence: 99%

“…In the latter these effects appear to be mediated by V2-receptors. Previous experiments have dealt with the cardiovascular action of exogenous vasopressin in normal rats, i.e. under conditions in which circulating, endogenous vasopressin could have influenced responses to the administered peptide (Hofbauer et al, 1983;Walker, 1986;Walker et al, 1988). In the present work we avoided this problem by investigating the regional haemodynamic effects of vasopressin infusion in conscious Brattleboro (i.e.…”

Section: Introductionmentioning

confidence: 99%

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Regional haemodynamic effects of vasopressin infusion in conscious, unrestrained, Brattleboro rats

Gardiner

Compton

Bennett

1989

British J Pharmacology

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“…Since Katusic & Krstic (1987) subsequently found that vasopressin caused endothelium-independent contractions of common carotid arteries from rats, they modified the earlier proposal (Katusic et al, 1984) by suggesting that a greater contractile response of renal than of common carotid arteries to vasopressin would favour cerebral perfusion when circulating vasopressin levels were raised. However, even under conditions in which sufficient vasopressin has been infused to cause substantial changes in cardiovascular variables we observed only a modest reduction in renal blood flow possibly due to concurrent activation of renal vasodilator mechanisms (Hofbauer et al, 1983;Walker et al, 1988). Moreover, in our previous study, although the changes in blood pressure and heart rate were similar to those seen with infusion of the higher dose of vasopressin in the present experiments, the increase in renal vascular resistance was only about half the increase in common carotid vascular resistance seen here.…”

Section: Discussionmentioning

confidence: 79%

The effects of infusions of arginine vasopressin or 1‐deamino‐8‐D‐arginine vasopressin on common carotid vascular resistance in conscious, Long Evans rats

Gardiner

Compton

Bennett

1989

British J Pharmacology

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1 Intravenous infusions of arginine vasopressin or 1-deamino-8-D-arginine vasopressin (DDAVP) were given to conscious, Long Evans rats chronically instrumented with bilateral, common carotid, pulsed Doppler probes and intravascular catheters. 2 During infusion of vasopressin at 0.3nmolmin1 there was an increase in common carotid vascular resistance with no change in mean blood pressure or heart rate. Following infusion there was a common carotid vasodilatation. 3 During infusion of vasopressin at 3.0 nmol min1 there were increases in mean arterial blood pressure and in common carotid vascular resistances, accompanied by bilateral reductions in flow and in heart rate. Administration of (+)-(CH2)5Tyr(Et)DAVP (a V1-receptor antagonist), during the continued infusion of vasopressin, reversed the effects of the latter on mean blood pressure and heart rate; under these conditions there were increases in common carotid blood flows above baseline, in company with bilateral vasodilatations. The latter effects persisted after cessation of vasopressin infusion.4 Infusions of DDAVP were without significant effects on any measured cardiovascular variable. 5 The results do not provide straightforward support for the claim that vasopressin acts to promote cerebral perfusion, at least when V1-receptor effects are unopposed. Furthermore, it seems likely that the vasodilator influence of vasopressin on the common carotid vascular bed is not due to stimulation of V2-receptors.

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Renal vascular effects of angiotensin II, arginine-vasopressin and bradykinin in rats: Interactions with prostaglandins

Cited by 21 publications

References 6 publications

Nitric oxide, but not vasopressin V2 receptor-mediated vasodilation, modulates vasopressin-induced renal vasoconstriction in rats

Nitric oxide, but not vasopressin V2 receptor-mediated vasodilation, modulates vasopressin-induced renal vasoconstriction in rats

Regional haemodynamic effects of vasopressin infusion in conscious, unrestrained, Brattleboro rats

The effects of infusions of arginine vasopressin or 1‐deamino‐8‐D‐arginine vasopressin on common carotid vascular resistance in conscious, Long Evans rats

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