Evidence for a Significant Contribution from Central Effects of Angiotensin in the Development of Acute Renal Hypertension in the Greyhound

1975 ◽  
Vol 48 (2) ◽  
pp. 115-119 ◽  
Author(s):  
G. C. Scroop ◽  
F. P. Katic ◽  
M. J. Brown ◽  
M. D. Cain ◽  
P. J. Zeegers
Keyword(s):  
Plasma Renin Activity ◽  
Renal Artery ◽  
Significant Role ◽  
Significant Contribution ◽  
Renal Hypertension ◽  
Plasma Renin ◽  
Renin Activity ◽  
Central Effects ◽  
Renal Artery Constriction

1. The importance of central vasomotor effects of endogenously generated angiotensin in the acute hypertensive response to renal artery constriction has been investigated in the anaesthetized greyhound. 2. When the central cardiovascular action of angiotensin was abolished by thermocoagulation of the areas postrema, the hypertensive response to renal artery constriction was reduced by half while the increase in plasma renin activity was unchanged. 3. It is concluded that central vasomotor effects of angiotensin play a significant role in renin-dependent hypertension.

Inhibition of angiotensin conversion and prevention of renal hypertension

1975 ◽  
Vol 228 (2) ◽  
pp. 448-453 ◽  
Author(s):  
Miller ED ◽  
AI Samuels ◽  
E Haber ◽  
AC Barger
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Renovascular Hypertension ◽  
Renal Hypertension ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Activity ◽  
Angiotensin System ◽  
The One ◽  
Renal Artery Constriction

Renal artery constriction in the unilaterally nephrectomized, trained dog, with maintained renal arterial hypotension, produces a prompt increase in systemic renin activity and blood pressure. The hypertension normally induced by renal artery stenosis is prevented by prior treatment with the nonapeptide Pyr-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro (SQ 20, 881), which blocks conversion of angiotensin I to angiotensin II. Constant intravenous infusion of the inhibitor over several days of renal artery constriction prevents the development of chronic renovascular hypertension. Furthermore, a single injection of the nonapeptide restores blood pressure to normal in the early phase of renovascular hypertension, but becomes progressively less effective as salt and water retention occurs in the chronic stage when plasma renin activity returns to control levels. These data provide strong evidence that the renin-angiotensin system is responsible for the initiation of renovascular hypertension in the one-kidney Goldblatt dog, but that other factors become increasingly important in chronic renovascular hypertension.

Salt and water balance and renin activity in renal hypertension of rats

1975 ◽  
Vol 228 (6) ◽  
pp. 1847-1855 ◽  
Author(s):  
J Mohring ◽  
B Mohring ◽  
H-J Naumann ◽  
A Philippi ◽  
E Homsy ◽  
...  
Keyword(s):  
Water Balance ◽  
Renal Artery ◽  
Renal Hypertension ◽  
The Body ◽  
Renin Activity ◽  
Sodium Balance ◽  
Sprague Dawley ◽  
Contralateral Kidney ◽  
Salt And Water Balance ◽  
Renal Artery Constriction

In male Sprague-Dawley rats, renal artery constriction in the presence of an inact contralateral kidney induced sodium retention (for 2-3 wk), moderate potassium loss,elevation of blood volume (BV), and an increase in water turnover. It is suggestedthat renal artery constriction activates the renin-angiotensin-aldosterone system, resulting in disordered regulation of salt and water balance and in blood pressure (BP) elevation. Subsequently, sodium balance was reestablished in one group of hypertensive rats. The previously retained sodium was kept in the body, and BV and reninactivity remained elevated. In a second group of animals, a malignant course of hypertension developed: BP surpassed a critical level of about 180 mmHg; sodium, potassium, and water were lost; BV declined; renin activity was further stimulated; and in the contralateral kidney malignant nephrosclerosis occurred. It is assumed that pressure diuresis and natriuresis induce a vicious circle: the increasing renin activity may maintain or further increase BP level, therby inducing further salt and water loss, etc.; high BP levels and high renin activities induce vascular damage and deterioration of renal function.

Renal Hypertension Due to Hydronephrosis with Normal Plasma Renin Activity

1970 ◽  
Vol 283 (19) ◽  
pp. 1032-1033 ◽  
Author(s):  
John M. Palmer ◽  
Franklin G. Zweiman ◽  
Tatiana A. Assaykeen
Keyword(s):  
Plasma Renin Activity ◽  
Renal Hypertension ◽  
Plasma Renin ◽  
Renin Activity ◽  
Normal Plasma

Plasma renin activity revealed renal artery stenosis concealed by aneurysms

Urology ◽  
2005 ◽  
Vol 65 (3) ◽  
pp. 592
Author(s):  
Masayuki Tanemoto ◽  
Takaaki Abe ◽  
Fumitoshi Satoh ◽  
Sadayoshi Ito
Keyword(s):  
Plasma Renin Activity ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Plasma Renin ◽  
Artery Stenosis ◽  
Renin Activity

EFFECTS OF EXPERIMENTAL RENAL HYPERTENSION ON ALDOSTERONE BIOSYNTHESIS BY RAT ADRENAL TISSUE

1969 ◽  
Vol 60 (4) ◽  
pp. 669-680 ◽  
Author(s):  
J. Müller ◽  
F. Gross
Keyword(s):  
Renal Artery ◽  
Renal Hypertension ◽  
Plasma Renin ◽  
Renin Activity ◽  
Sodium Deficiency ◽  
Marked Rise ◽  
Contralateral Kidney ◽  
Aldosterone Production ◽  
Experimental Renal Hypertension

ABSTRACT Aldosterone biosynthesis by quartered adrenal glands from rats with different forms of experimental renal hypertension due to clamping of one renal artery, was studied under various in vitro conditions. During incubation without aldosterone-stimulating substances, the adrenals of rats with one renal artery clamped and the other kidney left intact produced 200 % more aldosterone from endogenous precursors and converted 50 % more added tritium-labelled pregnenolone, progesterone or corticosterone to aldosterone than adrenals of control animals. The difference in aldosterone production was less marked when serotonin, KCl or ACTH was added to the incubation medium. The production of corticosterone and of deoxycorticosterone, respectively, was almost the same in adrenals of both groups of rats under most in vitro conditions. The marked rise in aldosterone production seen in the presence of an intact contralateral kidney was partially or completely inhibited, when simultaneously with renal artery constriction, the contralateral kidney was removed or the ureter of either the clamped or the contralateral kidney was ligated. These results indicate that in rats with experimental renal hypertension, increases in aldosterone production are correlated with increases of plasma renin activity and of the renin content of the clamped kidney, but are independent of changes in blood pressure. Since chronically elevated levels of plasma or renal renin activity act mainly in the early stages of aldosterone biosynthesis, it is concluded that the marked activation in the final stages of aldosterone biosynthesis observed in sodium deficiency is not mediated by the renin-angiotensin system.

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