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.

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.

EFFECT OF ADRENOCORTICOTROPHIC AND GROWTH HORMONES ON ALDOSTERONE PRODUCTION AND PLASMA RENIN ACTIVITY IN CHRONICALLY HYPOPHYSECTOMIZED SODIUM-DEFICIENT RATS

1970 ◽  
Vol 47 (2) ◽  
pp. 243-250 ◽  
Author(s):  
M. PALKOVITS ◽  
W. DE JONG ◽  
B. VAN DER WAL ◽  
D. DE WIED
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Normal Diet ◽  
Secretory Response ◽  
Renin Activity ◽  
Deficient Diet ◽  
Sodium Deficiency ◽  
Long Term Treatment ◽  
Aldosterone Production ◽  
Hypophysectomized Rats

SUMMARY Hypophysectomy abolishes the aldosterone secretory response to sodium deficiency in rats. Sodium deficiency causes a significant increase in plasma renin activity in chronically hypophysectomized rats which is of the same order as that found in intact animals. Long-term treatment with either adrenal maintenance doses of corticotrophin (ACTH) or with growth hormone (STH) did not affect the low rate of aldosterone production of hypophysectomized rats on a sodium-deficient diet. However, ACTH and STH given simultaneously restored the aldosterone secretory response to sodium deficiency in chronically hypophysectomized rats. The plasma renin activity of hypophysectomized rats on a sodium-deficient or a normal diet remained unaltered during treatment with either ACTH or STH or with the two hormones given simultaneously. This was also reflected in the systolic blood pressure of rats which, under the conditions used, did not change when the animals were sodium-deficient, or after hypophysectomy or hormone treatment. These results indicate that the effect of STH, in restoring the aldosterone secretory response to sodium deficiency in the presence of adrenal maintenance doses of ACTH in chronically hypophysectomized rats, is independent of changes in the renin-angiotensin system.

Renal Kallikrein Activity and Urinary Kallikrein Excretion in Rats with Experimental Renal Hypertension

1982 ◽  
Vol 63 (4) ◽  
pp. 349-354 ◽  
Author(s):  
M. Marin-Grez ◽  
G. Schaechtelin ◽  
G. Bönner ◽  
G. Speck ◽  
D. Ganten ◽  
...  
Keyword(s):  
Renal Hypertension ◽  
Plasma Renin ◽  
Renin Activity ◽  
Urinary Kallikrein ◽  
Hypertensive Rats ◽  
Control Value ◽  
Urinary Kallikrein Excretion ◽  
Renal Kallikrein ◽  
Experimental Renal Hypertension ◽  
Kallikrein Activity

1. Rats were made hypertensive by ligating the aorta between the origins of both renal arteries. Sham-operated animals served as controls. Urinary and renal kallikrein activities, as well as plasma and renal renin activities, were measured 8 and 90 days after surgery. 2. Blood pressure was 155 ± 6 mmHg on day 8 after aortic ligature and 142 ± 6 mmHg on day 90; in controls pressures were 107 ± 3 and 110 ± 5 mmHg respectively. 3. Eight days after aortic ligature, kallikrein activity in the ischaemic kidneys was about 6·5 times, and in the non-ischaemic kidneys almost 2 times, that in controls. After 90 days the kallikrein activity was reduced to one-half of that in the controls in the ischaemic kidneys and it was normal in the contralateral. 4. The urinary kallikrein excretion of hypertensive rats was about one-third of that of the controls at both 8 and 90 days after aortic ligature. 5. The plasma renin activity in hypertensive rats was approximately seven times that in control animals 8 days after aortic ligature and did not differ from the control value after 90 days. Renin activity in the kidneys showed the same pattern as in other models of renovascular hypertension: elevation in the ischaemic kidney and reduction in the non-ischaemic one.

The Vicious Circle in Acute Malignant Hypertension of Rats

1973 ◽  
Vol 45 (s1) ◽  
pp. 251s-255s ◽  
Author(s):  
G. Dauda ◽  
J. Möhring ◽  
K. G. Hofbauer ◽  
E. Homsy ◽  
Ulrike Miksche ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Hypertension ◽  
Plasma Renin ◽  
Malignant Hypertension ◽  
Hypertensive Rats ◽  
Marked Rise ◽  
Contralateral Kidney ◽  
Renal Hypertensive Rats ◽  
Malignant Nephrosclerosis ◽  
Drinking Fluid

1. In renal hypertensive rats, increase in blood pressure above 180 mmHg may induce sodium and water loss, reduced growth rate, elevated haematocrit, a marked rise in plasma renin concentration, an increase in renin extractable from the clamped and the contralateral kidney and malignant nephrosclerosis of the contralateral kidney. These symptoms characterize the malignant phase of renal hypertension in rats. 2. When water was given as drinking fluid, ten of eighteen rats developed signs of malignant hypertension and malignant nephrosclerosis within 3–4 weeks. Administration of 0.9% saline instead of water induced higher blood-pressure levels, but only five of eighteen rats showed malignant nephrosclerosis. When drinking fluid was changed from water to saline shortly before or shortly after the onset of malignant hypertension, the condition improved, and in only one of twelve rats was malignant nephrosclerosis observed. 3. It is concluded that in renal hypertensive rats sodium supplements may improve or prevent signs of malignant hypertension and the development of malignant nephrosclerosis.

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.

ALDOSTERONE AND CORTICOSTERONE PRODUCTION IN RENAL HYPERTENSIVE RATS

1975 ◽  
Vol 79 (2) ◽  
pp. 317-328 ◽  
Author(s):  
R. Dietz ◽  
G. J. Mast ◽  
J. Möhring ◽  
P. Vecsei ◽  
K. H. Gless ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Renal Hypertension ◽  
Plasma Concentrations ◽  
Plasma Aldosterone ◽  
Malignant Hypertension ◽  
Hypertensive Rats ◽  
Plasma Aldosterone Concentration ◽  
Contralateral Kidney ◽  
Aldosterone Production

ABSTRACT The development of hypertension, which had been elicited by clamping one renal artery in the presence of an untouched contralateral kidney, has been pursued in rats for up to six weeks after operation, and aldosterone and corticosterone production was studied at various intervals. Two weeks after renal artery stenosis had been induced, a "benign" and a "malignant" course of hypertension could be distinguished, the latter being characterized by a rise in blood pressure beyond 180–190 mmHg, loss of salt and water, increased water intake, decrease in body weight and food intake, and stimulation of the renin-angiotensin system. In the early phase of hypertension (after 9 days), aldosterone production and plasma aldosterone concentration were already elevated, and so was plasma corticosterone concentration. After 16 days, a marked increase in aldosterone production and in both plasma aldosterone and corticosterone concentrations was obtained in malignant hypertensive rats, whereas the secretion of the two hormones was only slightly stimulated in benign hypertensive rats. Similar differences in aldosterone production between rats with benign or malignant hypertension were found 21 and 42 days after operation. After 21 days, a close relationship between plasma renin concentration and aldosterone production was obtained in malignant hypertensive and control rats. A positive correlation between plasma concentrations of angiotensin II and of aldosterone was calculated for rats with malignant hypertension. It is concluded that, in the malignant phase of renal hypertension, a state of secondary aldosteronism develops as a consequence of negative sodium and water balance induced by high blood pressure.

Concentration of renin in kidneys and angiotensinogen in serum of various species

1960 ◽  
Vol 199 (5) ◽  
pp. 788-792 ◽  
Author(s):  
Carlos A. Schaffenburg ◽  
Erwin Haas ◽  
Harry Goldblatt
Keyword(s):  
Renal Hypertension ◽  
Human Kidney ◽  
Plasma Renin ◽  
Rabbit Kidney ◽  
High Concentration ◽  
Pronounced Increase ◽  
Experimental Renal Hypertension ◽  
Normal Human

In a study of the renin-angiotensinogen interaction, under various conditions of time, temperature and concentration of renin and angiotensinogen, an indirect method for the quantitative determination of renin in the kidneys and of angiotensinogen in the serum of nine species was developed. This method involves the bioassay of the angiotensin formed as a result of the incubation in vitro of purified renal extracts with homologous serum or plasma. Renin and angiotensinogen, at the concentrations of the latter existing in the serum of the various species, were both found to be rate-determining in the process of angiotensin formation. There were striking differences in the concentration of renin in normal kidneys of the various species, with rabbit kidney having more than 70 times as much renin as human kidney. A pronounced increase of renin was found in the ischemic kidney of dogs with experimental renal hypertension. An exceptionally high concentration of angiotensinogen was present in normal human serum compared to that of the eight other species investigated. The results of the previous and present determinations of the renin concentration in the kidneys of various species differ considerably because the former method depended upon a heterologous renin-angiotensinogen reaction, in vivo, while the present evaluation is based on a homologous renin-angiotensinogen reaction in vitro.

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.

Effects of calcium on renin and aldosterone in the rat.

1977 ◽  
Vol 232 (4) ◽  
pp. E388
Author(s):  
T A Kotchen ◽  
J H Galla ◽  
R G Luke
Keyword(s):  
Plasma Renin Activity ◽  
Calcium Gluconate ◽  
Plasma Renin ◽  
Renin Activity ◽  
Balance Study ◽  
Water Drinking ◽  
Aldosterone Production

CaCl2 suppresses the plasma renin activity (PRA) response to Na+ deprivation in the rat. The purpose of the present study is:1) to determine if the effect of Ca2+ on PRA is modified by the anion delivered with Ca2+, and 2) to evaluate the effect of Ca2+ loading on aldosterone production. PRA and in vitro aldosterone production by adrenal quarters were measured after a 7-day balance study. On a low Na+ diet, PRA of animals drinking 1% CaCl2 (13.1 ng/ml per h +/- 1.3 SE), but not of animals drinking 1% calcium gluconate, was suppressed (P less than 0.05) compared to that of water-drinking controls (20.9 ng/ml per h +/- 2.1 SE). Aldosterone production of calcium gluconate and CaCl2-loaded animals was greater than that of controls (P less than 0.01). K+ balance of CaCl2 and calcium gluconate-drinking animals was more positive than that of controls (P less than 0.05). In conclusion, inhibition of PRA by CaCl2 but not by calcium gluconate indicates that the effect of Ca2+ on PRA is modified by the accompanying anion. Both CaCl2 and calcium gluconate stimulate aldosterone production, independent of changes in PRA, possibly due to an effect of Ca2+ on K+ balance.

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