Journal ArticleDOI
Central Vasomotor Stimulation by Angiotensin
Carlos M. Ferrario,Carlos M. Ferrario,C. J. Dickinson,C. J. Dickinson,James W. Mccubbin,James W. Mccubbin +5 more
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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 bloodread more
Citations
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Journal ArticleDOI
Arginine vasopressin modulates the central action of angiotensin II in the dog.
TL;DR: Data demonstrate a previously unknown interaction between vasopressin and the centrally mediated pressor response to intravertebral AH, which is confined only to the cardiovascular response mediated by All via the vertebral arteries.
Book ChapterDOI
Central Neurogenic Effects of Angiotensin
TL;DR: The first section of this chapter is concerned with the neurogenic effects of renin or angiotensin, principally the facilitation of transmission in sympathetic ganglia and sensitization of the neurovascular effector in the postganglionic nerve terminals in such a way that the effects of locally released norepinephrine are augmented.
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Baroreceptor reflex in heart failure
TL;DR: In this article, a review on how baroreceptor reflex plays a role in abnormal control of the circulation in congestive heart failure is presented, which is a syndrome that is usually initiated by a reduction in pump function of the heart, i.e., a decrease in cardiac output.
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Clinical significance of hemodynamic findings in hypertension.
TL;DR: The description of pathophysiological alterations associated with the development of essential hypertension, hypertensive heart disease and renovascular hypertension are described and a rational basis for modern antihypertensive therapy is suggested.
Journal ArticleDOI
Location of the area postrema pressor pathway in the dog brain stem.
K L Barnes,C M Ferrario +1 more
TL;DR: Results suggest that the AP produces its facilitation of central sympathetic vasomotor outflow via a pathway contained within the medulla, rather than by fibers of passage from other pressor centers.
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
James W. Mccubbin,Irvine H. Page +1 more
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.
C. J. Dickinson,R. Yu +1 more
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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