Experimental Renal Hypertension: Renin Content of Kidneys in Intact and Adrenalectomized Rats Given Cortexone

1958 ◽  
Vol 195 (3) ◽  
pp. 543-548 ◽  
Author(s):  
F. Gross ◽  
P. Lichtlen
Keyword(s):  
Renal Artery ◽  
Renal Hypertension ◽  
Normal Animal ◽  
Renal Ischemia ◽  
Characteristic Distribution ◽  
Contralateral Kidney ◽  
Moderate Reduction ◽  
Small Doses ◽  
Experimental Renal Hypertension ◽  
Renin Content

The effects were investigated in rats of unilateral renal ischemia, adrenalectomy and varying doses of cortexone on the development of hypertension and on the content of pressor substances in the kidney. Adrenalectomy prevented the hypertension which follows unilateral clamping of the renal artery when a life maintaining dose of 0.1 mg cortexone acetate was injected daily. However, administration of 75 mg cortexone in the form of implants restored but did not enhance the characteristic hypertensive response to renal ischemia. The characteristic distribution of renal pressor material, being normal in the clamped and diminished in the contralateral kidney, was no longer observed after adrenalectomy when only small doses of cortexone were given but was still evident when excess cortexone was given. Overdosage with cortexone without clamping a renal artery led only to a moderate reduction of pressor material in both kidneys while in animals with unilateral renal ischemia the pressor material (renin?) in the contralateral kidney disappeared completely. Clamping the renal artery prevented the diminution of pressor material in the ipsilateral kidney which otherwise occurs under overdosage with cortexone in the normal animal.

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.

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.

Renin content and excretory function of the kidney in rats with experimental hypertension

1962 ◽  
Vol 202 (4) ◽  
pp. 795-799 ◽  
Author(s):  
H. Brunner ◽  
P. A. Desaulles ◽  
D. Regoli ◽  
F. Gross
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Renal Hypertension ◽  
Experimental Hypertension ◽  
Elevated Blood ◽  
Hypertensive Rats ◽  
Excretory Function ◽  
Contralateral Kidney ◽  
Ligation Of The Ureter ◽  
Renin Content

To determine relationship between kidney renin content and excretory function, rats with renal hypertension induced by unilateral clamping of the renal artery were given an oral load of 3 ml of 0.9% saline/100 g body wt. Excretion of the saline load was accelerated in rats with renal hypertension as well as in animals with hypertension due to overdosage with cortexone and salt, provided that the loading experiment was made 3–4 weeks after hypertension was established, but not when animals had been hypertensive for 11–14 weeks. Renin concentration was markedly reduced in the unclamped kidney and also in the kidney of the rats overdosed with cortexone and salt. Excreting capacity of the clamped kidney was compared with that of the unclamped kidney, after removal or after functional elimination of the contralateral kidney, by ligation of the ureter, 3, 24, and 48 hr after the operation. In all experiments excretion of saline load by the unclamped kidney was more rapid than by the clamped kidney, but the highest values were reached in the presence of a functional clamped kidney. Only in rats with elevated blood pressure was the load more rapidly excreted than in normal rats, but hypertension alone cannot be the only factor responsible, the excretion not being accelerated in unilaterally nephrectomized hypertensive rats. Although these hint at a connection between the renin concentration and renal function the nature of this relationship remains uncertain.

Development of chronic perinephritic hypertension in dogs without volume expansion

1977 ◽  
Vol 233 (4) ◽  
pp. F278-F281 ◽  
Author(s):  
R. H. Freeman ◽  
J. O. Davis ◽  
B. E. Watkins
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Volume Expansion ◽  
Left Kidney ◽  
Renal Hypertension ◽  
Control Level ◽  
Whole Body ◽  
Sodium Balance ◽  
Contralateral Kidney ◽  
Experimental Renal Hypertension

The theory of whole body autoregulation to explain the pathogenesis of experimental renal hypertension states that hypertension is initiated in response to an early increase in salt and water retention and a subsequent elevation of the cardiac output. This hypothesis was evaluated in the present study. Dogs (n,5) were made hypertensive by wrapping the left kidney in cellophane and removing the contralateral kidney 3 wk later. One week prior to right nephrectomy, the dogs were volume depleted by placing them on a low sodium intake (less than 3 meq of sodium/day) and giving them a mercurial diuretic for the first 3 days of the diet. This superimposed sodium depletion (negative sodium balance of 137 +/- 17 meq) increased plasma renin activity 3-5 times but did not change arterial pressure or heart rate. Within 2 days after nephrectomy, the mean arterial pressure increased from the control level of 105 +/- 1 to 135 +/- 6 mmHg (P less than 0.005) and pressure remained elevated throughout an additional 4-wk period in which volume depletion was enforced. The present study suggests, therefore, that initial blood volume expansion with such possible consequences as elevated cardiac output are not essential to the pathogenesis of experimental renal hypertension.

scholarly journals STUDIES ON EXPERIMENTAL HYPERTENSION

1943 ◽  
Vol 77 (4) ◽  
pp. 297-307 ◽  
Author(s):  
Harry Goldblatt ◽  
Joseph R. Kahn ◽  
Harvey A. Lewis
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Renal Hypertension ◽  
Renal Arteries ◽  
Experimental Hypertension ◽  
Long Duration ◽  
Humoral Mechanism ◽  
Main Renal Artery ◽  
Experimental Renal Hypertension ◽  
The One

Persistent hypertension has been produced in the goat and sheep by constriction of the main renal arteries. The presence or absence of accompanying uremia depends upon the degree of constriction of the renal arteries. In both sheep and goat, constriction of one main renal artery also caused elevation of the blood pressure which tended to persist longer than in the dog. Excision of the one kidney with main renal artery constricted resulted in a prompt (24 hours) return of the blood pressure to normal. In the animals with hypertension of long duration but without renal excretory insufficiency, (the "benign" phase) no significant arterio- or arteriolosclerosis developed as a result of the hypertension alone. In the animals that had both hypertension and renal excretory insufficiency, (the "malignant" phase) the typical terminal arteriolar lesions developed in many organs. These lesions consisted of necrosis and fibrinoid degeneration of arterioles and necrotizing arteriolitis which should not be confused with arteriolosclerosis. The same humoral mechanism which is responsible for experimental renal hypertension in the dog and other animals also obtains in the pathogenesis of experimental renal hypertension in the sheep and goat.

ALDOSTERONE AND CORTICOSTERONE SECRETION RATES IN RATS WITH EXPERIMENTAL RENAL HYPERTENSION

1963 ◽  
Vol 44 (4) ◽  
pp. 505-518 ◽  
Author(s):  
Bertha Singer ◽  
Carine Losito ◽  
Sheila Salmon
Keyword(s):  
Renal Artery ◽  
Renal Hypertension ◽  
Secretion Rate ◽  
The Other ◽  
Blood Collection ◽  
Aldosterone Secretion ◽  
Negative Results ◽  
Corticosterone Secretion ◽  
Experimental Renal Hypertension ◽  
Secretion Rates

ABSTRACT In animals with one renal artery clip hypertension was associated with a highly significant increase in aldosterone but not corticosterone secretion rate. In unilaterally nephrcctomized animals with a clip on the remaining renal artery, hypertension was not associated with a significant change in the secretion rates of aldosterone or corticosterone. Experiments designed to determine whether this difference in the groups was due to the fact that in the first group the 'clipped' kidney was still in the circulation during blood collection while in the second it was not have yielded essentially negative results. It is concluded that the increase in aldosterone secretion in renal hypertension is related to the response of the untouched kidney to the clamping of the renal artery of the other kidney.

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