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Journal ArticleDOI

Central Vasomotor Stimulation by Angiotensin

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TLDR
Angiotensin was infused at low rates into the vertebral arteries of anaesthetized dogs, and when infused at similar rates intravenously or into the internal carotid artery it either did not change blood pressure, or raised it only very slightly, suggesting that part of the pressor effect of intravenous ang Elliotensin may be mediated by a direct stimulation of some parts of the hind brain.
Abstract
SUMMARY 1. When angiotensin was infused at low rates into the vertebral arteries of anaesthetized dogs, it raised the blood pressure. When infused at similar rates intravenously or into the internal carotid artery it either did not change blood pressure, or raised it only very slightly. The difference in response was highly significant over the range of 1-50 ng kg- ' min- '. 2. During intravenous infusion at higher rates, angiotensin usually produced the well-known reflex bradycardia and fall of cardiac output, but on infusion into the vertebral arteries it rapidly raised systemic arterial pressure, often increased heart rate, and usually produced a transient increase of cardiac output. 3. Angiotensin by both routes raised peripheral resistance, but noradrenaline, by contrast, produced the same response whether it was given into the vertebral arteries or into a vein. 4. These observations suggest that part of the pressor effect of intravenous angiotensin may be mediated by a direct stimulation of some part of the hind brain. There are several means by which angiotensin may raise systemic arterial pressure. In addition to its direct arterial vasoconstrictor action, it can release catecholamines from the adrenal medulla (Braun-Menhdez, Fasciolo, Leloir & Muiioz, 1940), stimulate or facilitate transmission in sympathetic ganglia (Lewis & Reit, 1966) and enhance the peripheral vasoconstrictor response to endogenously released noradrenaline (McCubbin & Page, 1963a, b). In very large doses it was reported, 9 years ago, to cause central stimulation of the sympatho-adrenal system when infused into the the dog's cerebral circulation which was isolated and perfused from another animal (Bickerton & Buckley, 1961). The special importance of the vertebral artery territory in mediating the central stimulatory effects of angiotensin, and the extreme sensitivity to angiotensin when given into the vertebral artery, was first observed in conscious rabbits (Dickinson, 1965; Yu & Dickinson, 1965) and in anaesthetized rabbits after blood

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Citations
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Journal ArticleDOI

Neurogenic actions of angiotensin II.

C M Ferrario
- 01 Nov 1983 - 
TL;DR: The role of angiotensin II in the regulation of central adrenoreceptor activity, pituitary function, and hydromineral metabolism was reviewed in this article, and a framework for future research is suggested by the author.
Journal ArticleDOI

Role of the renin-angiotensin system in the control of vasopressin secretion in conscious dogs.

TL;DR: The results suggest that endogenous angiotensin II may be necessary for the maintenance of normal baroreflex control of vasopressin secretion during sodium depletion.
Journal ArticleDOI

Restoration of suppressed baroreflex sensitivity in rats with hereditary diabetes insipidus (Brattleboro rats) by arginine-vasopressin and DDAVP.

TL;DR: The results obtained in Brattleboro rats and the change in baroreflex sensitivity brought about by infusions of vasopressin and DDAVP provide strong evidence that vasoppressin may be an important physiological modulator of barore Flex function.
Journal ArticleDOI

Angiotensin-converting enzyme inhibitor resets baroreceptor reflexes in conscious dogs.

TL;DR: It is indicated that circulating but not brain angiotensin II is essential for the maintenance of baroreflex function during sodium depletion and provide further evidence for the important Interactions between ang Elliotensin and the autonomic nervous system.
Journal ArticleDOI

Long-term control of congestive heart failure with captopril

TL;DR: It is suggested that the response of congestive heart failure to captopril can occur gradually and improvement was related to peripheral hemodynamic changes which led to a reduction in both total peripheral resistance and cardiopulmonary volume.
References
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Journal ArticleDOI

Evidence for a Central Mechanism in Angiotensin Induced Hypertension.

TL;DR: Angiotensin II appears to produce an increase in blood pressure by a central hypertensive effect, probably due to stimulation of central sympathetic structures and evoking peripheral sympathetic discharges, which is blocked by administration of a sympatholytic agent into the peripheral circulation.
Journal ArticleDOI

Renal Pressor System and Neurogenic Control of Arterial Pressure

TL;DR: By intensifying the effect of normal neurogenic vasomotor activity, this action of angiotensin, along with the upward shift of threshold and range of response of the carotid sinus buffer mechanism, might account to a major degree for the large neurogenic component of chronic renal hypertension.
Journal ArticleDOI

The progressive pressor response to angiotensin in the rabbit.

TL;DR: The threshold for any detectable rise of systemic arterial pressure during the prolonged intravenous administration of angiotensin to conscious rabbits was observed to be an infusion rate of 0·003‐0·006 μg.
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