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The progressive pressor response to angiotensin in the rabbit.

C. J. Dickinson, +1 more
- 01 May 1967 - 
- Vol. 190, Iss: 1, pp 91-99
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TLDR
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.
Abstract
1. 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.kg−1.min−1. 2. At infusion rates between threshold and 0·04 μg.kg−1.min−1 the systemic arterial pressure rose progressively over a 3- to 7-day period to a plateau. 3. On stopping the angiotensin infusion the blood pressure fell rapidly back to its base line much faster than it rose during the infusion. The time taken to reach control values was approximately related to the duration of the infusion. 4. At infusion rates of about 0·05 μg.kg−1.min−1 the full rise of blood pressure developed within a few minutes, and could be sustained without change for many days. At higher rates the blood pressure diminished with time. 5. Diurnal fluctuations of blood pressure were often seen during prolonged infusions of angiotensin at low rates; and more rapid fluctuations of blood pressure over an hour or two were frequently encountered immediately after an infusion was turned off. 6. The possible role of angiotensin in producing chronic renal hypertension is discussed in the light of these observations.

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Citations
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Journal ArticleDOI

Central Vasomotor Stimulation by Angiotensin

TL;DR: 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.
Journal ArticleDOI

Angiotensin ii blood-levels in human hypertension

TL;DR: It is proposed that high levels of circulating angiotensin II may contribute to the development of renal hypertension in man, and that the ability of the diseased kidney to compensate for the pressor effects of high angiotENSin levels by adjusting sodium and fluid balance may be an additional determining factor in theDevelopment of hypertension associated with renal disease.
Journal ArticleDOI

Quantification of baroreceptor influence on arterial pressure changes seen in primary angiotension-induced hypertension in dogs.

A W Cowley, +1 more
- 01 Dec 1976 - 
TL;DR: It is concluded that the final 30% increase in pressure seems to result from increased cardiac output, the cause of which may be decreased vascular compliance, since the blood volume remains unaltered.
Journal ArticleDOI

Sensitization of Slow Pressor Angiotensin II (Ang II)–Initiated Hypertension: Induction of Sensitization by Prior Ang II Treatment

TL;DR: Results indicate that subpressor doses of Ang II act on the brain to sensitize the hypertensive response to subsequent Ang II and that sensitization is associated with altered expression of RAAS components in forebrain cardiovascular control structures.
OtherDOI

Renin–Angiotensin–Aldosterone System and the Renal Regulation of Sodium, Potassium, and Blood Pressure Homeostasis

TL;DR: The sections in this article are: A Coordinated Renal-Adrenal Hormonal System: Renin, Angiotensin, and Aldosterone, and Human Disorders of the Renin System.
References
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Journal ArticleDOI

Arterial Hypertension Elicited by Subpressor Amounts of Angiotensin

TL;DR: This indirect action of angiotensin to increase total peripheral resistance and arterial pressure by an action on the sympathetic nervous system, along with an upward resetting of the carotid sinus buffering mechanism, might logically account for the neural component of chronic renal hypertension.
Journal ArticleDOI

Bio-assay of circulating renin-like pressor material by isovolemic cross circulation.

TL;DR: There is a good correlation between the concentration of renin in the kidney and of pressor material in the blood, while the level of circulating renin-like substance is not correlated with the height of blood pressure.
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