Oestrogen Hypertension in Rats

1975 ◽  
Vol 48 (5) ◽  
pp. 457-460
Author(s):  
T. Saruta ◽  
R. Nakamura ◽  
I. Saito ◽  
K. Kondo ◽  
S. Matuki

1. A large dose of oestrogen elevated the blood pressure in male Wistar rats. 2. Plasma renin substrate and renin activity increased significantly but plasma renin concentration was unchanged. 3. The increase in blood pressure induced by oestrogen was significantly reduced by salt loading, plasma renin concentration was suppressed and the increase in plasma renin activity was reduced. 4. The increase in plasma renin activity induced by the increase of plasma renin substrate concentration may play a role in oestrogen-induced elevation of blood pressure.

1973 ◽  
Vol 45 (s1) ◽  
pp. 287s-290s
Author(s):  
C. I. Johnston ◽  
N. Anavekar ◽  
K. G. Chua ◽  
W. J. Louis

1. The levels of plasma renin activity or concentration and plasma angiotensin were similar in normotensive subjects and in untreated or treated essential hypertensives. 2. There was a close relationship between plasma renin activity and plasma renin concentration and between these and plasma angiotensin. This suggests that there were no abnormalities in renin substrate or renin kinetics in human essential hypertension. 3. Ganglion blockade did not change the plasma renin levels but α-adrenergic blockade caused a significant rise in plasma catecholamines and plasma renin without change in blood pressure. 4. Both acute and chronic β-adrenergic blockade were associated with a fall in blood pressure and small but significant falls in plasma renin levels.


1984 ◽  
Vol 16 (06) ◽  
pp. 315-318 ◽  
Author(s):  
E. Jiménez ◽  
M. Montiel ◽  
J. Narváez ◽  
M. Miranda ◽  
L. Parras ◽  
...  

1975 ◽  
Vol 48 (2) ◽  
pp. 147-151
Author(s):  
C. S. Sweet ◽  
M. Mandradjieff

1. Renal hypertensive dogs were treated with hydrochlorothiazide (8−2 μmol/kg or 33 μmol/kg daily for 7 days), or timolol (4.6 μmol/kg daily for 4 days), a potent β-adrenergic blocking agent, or combinations of these drugs). Changes in mean arterial blood pressure and plasma renin activity were measured over the treatment period. 2. Neither drug significantly lowered arterial blood pressure when administered alone. Plasma renin activity, which did not change during treatment with timolol, was substantially elevated during treatment with hydrochlorothiazide. 3. When timolol was administered concomitantly with hydrochlorothiazide, plasma renin activity was suppressed and blood pressure was significantly lowered. 4. These observations suggest that compensatory activation of the renin-angiotensin system limits the antihypertensive activity of hydrochlorothiazide in renal hypertensive dogs and suppression of diuretic-induced renin release by timolol unmasks the antihypertensive effect of the diuretic.


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