Effects of Sex Hormones on the Renal Pressor System

1971 ◽  
Vol 49 (4) ◽  
pp. 292-301 ◽  
Author(s):  
Alberto Nasjletti ◽  
Masato Matsunaga ◽  
Georges M. C. Masson
Keyword(s):  
Plasma Renin Activity ◽  
Sex Hormones ◽  
Negative Feedback ◽  
Substrate Concentration ◽  
Renal Hypertension ◽  
Plasma Renin ◽  
Renin Activity ◽  
High Substrate Concentration ◽  
High Substrate ◽  
Constant Dose

The effects of sex and sex hormones on angiotensinogen, renin activity, and renin concentration in plasma and on renal renin were investigated in rats. During estrus there was a significant increase in angiotensinogen, which was suppressed by ovariectomy. In males, castration had no effect. Administration of stilbestrol caused a rapid increase in angiotensinogen. Renal renin and plasma renin concentration decreased while plasma renin activity remained near normal levels. Following addition of a constant dose of rat renin, plasma from estrogen-treated rats released angiotensin at a faster rate than normal plasma; this increased reactivity is attributed to the high substrate concentration and not to the lack of an inhibitor, to the presence of an activator, or of a more reactive substrate. These changes were not modified by progesterone or testosterone. Progesterone alone caused a significant increase in renal renin. Estrogens did not elicit hypertension nor modify a preexisting renal hypertension. These observations support the hypothesis that the primary effect of estrogens is an increased angiotensinogen formation, and that the resulting enhancement in plasma reactivity to renin causes an increase in angiotensin which acts as a negative feedback on renin production.

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

Renal venous and peripheral plasma renin activity in renal hypertension in the rat

1973 ◽  
Vol 225 (6) ◽  
pp. 1513-1518 ◽  
Author(s):  
FH Leenen ◽  
W de Jong ◽  
D de Wied
Keyword(s):  
Plasma Renin Activity ◽  
Renal Hypertension ◽  
Plasma Renin ◽  
Renin Activity ◽  
Peripheral Plasma

CIRCULATORY RESPONSES, PLASMA RENIN ACTIVITY AND KININOGEN IN RATS WITH RENAL HYPERTENSION

Abstracts ◽  
1978 ◽  
pp. 378
Author(s):  
P. Säynävälammi ◽  
A. Raitanen ◽  
J. Olkoniemi ◽  
T. Pohjolainen ◽  
M.-L. Pyykönen ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Renal Hypertension ◽  
Plasma Renin ◽  
Renin Activity

Effects of Salt and Water Depletion on the Early Phase of Hypertension in Goldblatt two-Kidney Hypertensive Dogs

1981 ◽  
Vol 60 (6) ◽  
pp. 625-631
Author(s):  
M. L. Watson ◽  
J. McCormick ◽  
A. Thom ◽  
P. Whelpdale ◽  
A. Ungar
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Sodium Intake ◽  
Renal Hypertension ◽  
Plasma Renin ◽  
Renin Activity ◽  
Prostaglandin E ◽  
Sodium Restriction ◽  
Arterial Plasma ◽  
Venous Plasma

1. Hypertension was induced in dogs by partial occulsion of one renal artery, the opposite kidney remaining intact, and the changes in blood pressure, plasma renin activity, aldosterone and prostaglandin E (PGE) were monitored. 2. Two days after induction of hypertension, the retained sodium and water were removed by haemodialysis and the animals were then maintained on a low dietary intake of sodium for the following 7 days. 3. Removal of the accumulated sodium and water had no immediate effect on blood pressure, but during the ensuing 7 days there was a small decrease in blood pressure, which again increased after re-institution of a normal sodium intake. 4. Plasma renin activity and aldosterone increased during development of hypertension and remained elevated during the period of sodium restriction. 5. Sodium and water retained during the development of hypertension was not responsible for the elevated blood pressure. 6. The concentration of PGE in arterial plasma and renal venous plasma from the undamped kidney were unchanged during the study, although we have previously shown that in the absence of sodium depletion, PGE rises. 7. PGE released from the kidney may be important in mediating the excretion of sodium and water that is retained during the development of renal hypertension.

Changes in the Renin-Angiotensin-Aldosterone System and in Sodium and Potassium Balance during Development of Renal Hypertension in Rats

1975 ◽  
Vol 48 (1) ◽  
pp. 17-26 ◽  
Author(s):  
F. H. H. Leenen ◽  
J. W. Scheeren ◽  
D. Omylanowski ◽  
J. D. Elema ◽  
B. Van Der Wal ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Systolic Blood Pressure ◽  
Renal Hypertension ◽  
Plasma Renin ◽  
Renin Activity ◽  
Hypertensive Rats ◽  
Potassium Balance ◽  
Peripheral Plasma ◽  
Sodium And Potassium

1. The relationships between the renin-angiotensin-aldosterone system, sodium and potassium balance and systolic blood pressure were studied during development of moderate (160–180 mmHg; clip i.d. 0.25 mm) and severe (200–230 mmHg; clip i.d. 0.20 mm) renal hypertension in rats with an undisturbed contralateral kidney. 2. In severely hypertensive rats renin activity in the peripheral plasma increased from day 9, by which time the systolic blood pressure was elevated to 160–180 mmHg. The rate of total corticosteroid and aldosterone production in vitro increased from day 14 and plasma renin substrate concentration increased from day 24. In moderately hypertensive rats, none of these changes occurred. 3. During the first 10 days after the application of 0.25 and 0.20 mm clips, sodium and potassium retention/g gain in body weight were higher than in sham-operated controls. During the next 10 days, the positive balance stabilized in animals with a 0.25 mm clip whereas, in animals with a 0.20 mm clip, sodium and potassium balance returned to the level of the sham-operated controls through increased renal losses. Despite these changes the systolic pressure rose further in animals with a 0.20 mm clip. 4. The initial sodium retention could be a factor in the early rise of blood pressure and could account for the delay in the rise of peripheral plasma renin activity. The subsequent loss of the retained sodium and potassium during the development of severe hypertension could have facilitated the rise in peripheral plasma renin activity, but did not initiate this rise.

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