Glucocorticoid Inhibition of Mineralocorticoid Action in the Rat

1984 ◽  
Vol 67 (3) ◽  
pp. 329-335 ◽  
Author(s):  
C. J. Kenyon ◽  
N. A. Saccoccio ◽  
D. J. Morris
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Long Term Effects ◽  
Physiological Dose ◽  
Acute Changes ◽  
Adrenalectomized Rats

1. The mineralocorticoid activity of corticosterone based on acute changes in urinary Na+/K+ ratios in adrenalectomized rats was 1000 times less than that of aldosterone. However, corticosterone had only kaliuretic actions whereas aldosterone had both antinatriuretic and kaliuretic properties. Corticosterone inhibited the antinatriuretic actions of aldosterone. 2. Adrenalectomized rats infused continuously with a physiological dose of corticosterone (1 mg/day) were 5 times less sensitive to the antinatriuretic and 25 times less sensitive to the kaliuretic actions of aldosterone when administered acutely than were control adrenalectomized rats. 3. The long term effects of infusions of physiological doses of aldosterone and corticosterone were assessed in adrenalectomized rats maintained in metabolic cages. Aldosterone lowered plasma renin activity and reduced fluid (0.3% NaCl) intake; these effects were diminished when aldosterone and corticosterone were infused simultaneously. Plasma renin activity and fluid intake were correlated in long term infusion experiments. Both hormones had hypokalaemic effects but these were not additive. Corticosterone, but not aldosterone, increased systolic blood pressure and plasma sodium levels. 4. We conclude that glucocorticoid effects on water and electrolyte metabolism are different from those of mineralocorticoids, that glucocorticoids may antagonize mineralocorticoid effects and that interactions between mineralocorticoids and glucocorticoids may be important in long term blood pressure regulation.

Arterial pressure after chronic reductions in suprarenal aortic flow in fetal lambs

1987 ◽  
Vol 253 (4) ◽  
pp. H838-H844
Author(s):  
D. F. Anderson ◽  
C. M. Parks ◽  
J. J. Faber
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Arterial Blood Pressure ◽  
Plasma Renin ◽  
Aortic Flow ◽  
Renin Activity ◽  
Upper Body ◽  
Aortic Blood Flow ◽  
Arterial Blood

Experiments were performed on 13 fetal lambs of 126 days gestational age. Seven days after surgery, suprarenal aortic blood flow was reduced to 70% of control with an inflatable occluder for a period of at least 4 days. This produced an almost constant aortic pressure difference of 35 mmHg across the occluder. Plasma renin activity (PRA) rose in the next hour from 6 to 42 ng.ml-1.h-1 (P less than 0.01) but decreased to a level that was statistically insignificantly above normal by the next day. PRA as a function of lower body arterial blood pressure showed rapid adaptation. Upper body arterial blood pressure was statistically significantly elevated by 5 mmHg within 5 min and continued to rise while plasma renin activity was falling. Femoral artery blood pressure dropped immediately but returned to near normal within 1 h and remained there. The long-term upper body hypertension was irreversible with a 30-min infusion of saralasin. Subrenal aortic flow reduction caused none of these changes. We conclude that the fetal kidneys can regulate arterial blood pressure upward but that the long-term effect does not depend solely on a direct vasoconstrictive action of angiotensin.

Long-Term Propranolol Treatment of Resistant Arterial Hypertension in Haemodialysed Patients

1974 ◽  
Vol 48 (s2) ◽  
pp. 73s-75s
Author(s):  
Q. Maggiore ◽  
M. Biagini ◽  
C. Zoccali ◽  
M. Misefari
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Arterial Hypertension ◽  
Plasma Renin ◽  
Renin Activity ◽  
Term Basis ◽  
Excellent Control ◽  
Propranolol Treatment ◽  
Resistant Arterial Hypertension

1. Propranolol was given to eight haemodialysed patients with resistant arterial hypertension for periods ranging from 6 to 16 months. 2. The treatment brought about an excellent control of blood pressure in all cases. 3. After withdrawal of propranolol plasma renin activity rose on average 40% compared with the value obtained during treatment. However, no significant relationship was found between the change in plasma renin activity and the change in the diastolic blood pressure. 4. Stopping propranolol resulted in a prompt rebound of arterial pressure toward pretreatment values. However, hypertension was always controlled on resuming drug treatment. 5. The results show that this form of hypertension can be controlled on a long-term basis with propranolol. However, the effect on blood pressure seems not to be mediated by suppression of renin secretion.

Enhancement of the Antihypertensive Effect of Hydrochlorothiazide in Dogs after Suppression of Renin Release by Beta-Adrenergic Blockade

1975 ◽  
Vol 48 (2) ◽  
pp. 147-151
Author(s):  
C. S. Sweet ◽  
M. Mandradjieff
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Arterial Blood Pressure ◽  
Antihypertensive Effect ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Antihypertensive Activity ◽  
Adrenergic Blockade ◽  
Arterial Blood

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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