Action of Angiotensin on Sympathetic Nerve Endings in Isolated Blood Vessels

Distler, A.; Liebau, H.; Hp, Wolff

doi:10.1038/207764a0

Cited by 56 publications

(11 citation statements)

References 4 publications

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“…The interaction between glucagon and specific angiotensin receptors may conform to this pattern, but in addition there is the observation that angiotensin interacts with adrenergic nerve terminals, enhancing and possibly even stimulating the release of the transmitter (Distler, Liebau & Wolff, 1965;Regoli, Park & Rioux, 1974). The interaction of angiotensin and glucagon might, therefore be expected to conform closely to the characteristics of noradrenaline/ glucagon interaction if a major component of the action of angiotensin involves an effect on the adrenergic nerve terminal.…”

Section: Discussionmentioning

confidence: 99%

The Inhibition by Glucagon of the Vasoconstrictor Actions of Noradrenaline, Angiotensin and Vasopressin on the Hepatic Arterial Vascular Bed of the Dog

Richardson

Withrington

1976

British J Pharmacology

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I The hepatic artery of the anaesthetized dog was cannulated and perfused from a femoral artery, the blood flow and perfusion pressure being monitored continuously. The sympathetic periarterial nerves were divided. 2 Dose-dependent increases in hepatic arterial vascular resistance (HAVR) resulted from intraarterial injections of noradrenaline, angiotensin and vasopressin. 3 Single injections of glucagon (100 gg, i.a.) caused a transient significant fall in HAVR of 19.9 + 3.2%, and infusions of 25 tg/min of glucagon intra-arterially caused maintained reductions in HAVR of 16.9 + 4.2%. 4 After single injections of 100 gg glucagon intra-arterially the vasoconstrictor responses to noradrenaline, angiotensin, and vasopressin were reduced by about 85-95%. Recovery occurred in 8-10 minutes. 5 Intra-arterial infusions of glucagon, 2.5-50.0,g/min, reduced the effects of test doses of noradrenaline, angiotensin and vasopressin throughout the period of the infusions. 6 Dose-response curves to the constrictor agents were constructed before, during and after intraarterial infusions of 25 gg/min of glucagon. Glucagon caused a parallel shift of the curves for noradrenaline and angiotensin to the right, with no suppression of the maximum response. 7 Infusions of glucagon shifted the dose-response curve for vasopressin to the right, but, in contrast to noradrenaline and angiotensin, the shift was nonparallel and there was a suppression of the maximum response by about one-half. 8 A large dose of insulin, 10 iu, transiently reduced HAVR and caused a weak and very transient inhibition of the effect of test doses of noradrenaline. The characteristics of these effects were quite different from those of glucagon. 9 It is possible that the antagonism by glucagon of the vasoconstrictor responses of the hepatic arterial vasculature may be important in protecting this vascular bed from the effects of concomitantly released vasoconstrictor agents.

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Section: Discussionmentioning

confidence: 99%

The Inhibition by Glucagon of the Vasoconstrictor Actions of Noradrenaline, Angiotensin and Vasopressin on the Hepatic Arterial Vascular Bed of the Dog

Richardson

Withrington

1976

British J Pharmacology

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“…One postulates that it is due to the long-lasting occupancy of the angiotensin receptors by the agonist. The other theory explains tachyphylaxis as a consequence of the exhaustion of a hypothetical secondary messenger of angiotensin such as catecholamines and prostaglandins (Distler et al 1965;Aiken 1974).Recently, a new method (cannula inserting method) for perfusing isolated arteries was developed by Hongo and Chiba (1983) and modified by Tsuji and Chiba (1984). By use of this method, vascular responses of isolated mesenteric arteries to vasoactive substances were widely investigated (Chiba and Tsukada…”

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confidence: 99%

Angiotensin II-induced tachyphylactic constrictions in isolated and perfused canine mesenteric arteries.

Chiba

Tsukada

1986

Tohoku J. Exp. Med.

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The stainless steel cannula inserting method was used to investigate the effects of angiotensin II on isolated and perfused dog mesenteric arteries with and without indomethacin treatment, or with and without intraluminal saponin-treatment which removed the endothelium. In non-treated preparations, angiotensin II was intraluminally administered repetitively at 10, 20, 30 or 60 min inervals. Each period of angiotensin II causes tachyphylaxis. The order of degree of tachyphylaxis was 10>20>30>60 min intervals. Relatively large doses much readily caused tachyphylaxis. Tachyphylaxis was not affected by phentolamine-treatment preparations. In indomethacin (5 mg)-treated preparations, the angiotensin II-induced tachyphylaxis was significantly less than that in non-treated ones. In small doses of angiotensin II, tachyphylaxis did not appear in the majority of cases in indomethacin-treated preparations. In deendothelial preparations which were induced by intraluminal administration of saponin (1 and 3 mg), the tachyphylaxis was induced similar to non-saponin treated preparations. It is concluded that 1) prostaglandin may partially participate in induction of angiotensin-induced tachyphylaxis, 2) the prostaglandin may be synthesized in the inside of vasculature, and 3) a large dose of angiotensin II induces tachyphylaxis unrelated to production of prostaglandin. dog mesenteric artery ; cannula inserting method ; angiotensin II; indomethacin Angiotensin-induced tachyphylaxis has been well known in isolated preparations of vascular and non-vascular smooth muscle as reviewed by Page and Bumpus (1961). Two theories were proposed on angiotensin tachyphylaxis. One postulates that it is due to the long-lasting occupancy of the angiotensin receptors by the agonist. The other theory explains tachyphylaxis as a consequence of the exhaustion of a hypothetical secondary messenger of angiotensin such as catecholamines and prostaglandins (Distler et al. 1965;Aiken 1974).Recently, a new method (cannula inserting method) for perfusing isolated arteries was developed by Hongo and Chiba (1983) and modified by Tsuji and Chiba (1984). By use of this method, vascular responses of isolated mesenteric arteries to vasoactive substances were widely investigated (Chiba and Tsukada

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“…It is well kown that captopril is an angiotensin-converting enzyme inhibitor and inhibits production of angiotensin II, which induces direct vasoconstriction, secretion of aldosterone, secretion of vasopressin (Mouw et al, 1971;KEIL et al, 1975;SUZUKI et a!., 1982), release of catecholamine from sympathetic nerve endings (DISTER et al, 1965;KIRAN and KHAIRALLAH, 1969), and enhancement of the sympathetic system mediated by stimulation of the cardiovascular center (UNDER et al, 1981). Captopril also induces reduction of the total peripheral resistance with the lowering of arterial pressure in essential hypertension (FUJITANI et al, 1979;TARAZI et a!.,1980).…”

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Acute effects of captopril on blood pressure and regional blood flows in two types of renovascular hypertensive rats in conscious state.

1988

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Mean arterial pressure and three regional blood flows-renal, superior mesenteric, and hindquarter flows-were monitored in conscious normotensive control rats (NCR), in two-kidney, one-clip (two-kidney), and in one-kidney, one-clip (one-kidney) hypertensive rats. After administering captopril, an angiotensin-converting enzyme inhibitor, mean arterial pressure decreased in all three groups. However, lowering of arterial pressure was not statistically significant in any of the groups. Renal flow increased significantly in the intact artery of two-kidney hypertensive rats, whereas it did not significantly increase in the clipped artery of one-kidney hypertensive rats and in the intact artery of NCR. Superior mesenteric flow increased significantly only in one-kidney hypertensive rats. Hindquarter flow did not significantly change in the three groups. Regional resistance reduced significantly in not only renal but also in superior mesenteric vascular area in two-kidney hypertensive rats, whereas it did not reduce significantly in these two vascular areas in one-kidney hypertensive rats and in NCR. The present findings show that the reninangiotensin-mediated vasoconstriction plays a role in not only renal but also in superior mesenteric vascular area in two-kidney hypertensive rats, whereas it hardly plays a role in these three vascular beds in one-kidney hypertensive rats.

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Action of Angiotensin on Sympathetic Nerve Endings in Isolated Blood Vessels

Cited by 56 publications

References 4 publications

The Inhibition by Glucagon of the Vasoconstrictor Actions of Noradrenaline, Angiotensin and Vasopressin on the Hepatic Arterial Vascular Bed of the Dog

The Inhibition by Glucagon of the Vasoconstrictor Actions of Noradrenaline, Angiotensin and Vasopressin on the Hepatic Arterial Vascular Bed of the Dog

Angiotensin II-induced tachyphylactic constrictions in isolated and perfused canine mesenteric arteries.

Acute effects of captopril on blood pressure and regional blood flows in two types of renovascular hypertensive rats in conscious state.

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