Effects of Prazosin on Blood Pressure and Plasma Renin Activity in Man

1978 ◽  
Vol 55 (s4) ◽  
pp. 337s-339s
Author(s):  
J. Rosenthal ◽  
H. Jaeger ◽  
I. Arlart

1. The effects of oral administration of 4·5 mg of prazosin/day on blood pressure and on plasma renin activity were assessed in patients with essential hypertension and in healthy normotensive volunteer subjects. 2. Mean blood pressure in the hypertensive group fell significantly within 2 weeks of treatment, whereas heart rate was little affected. None of the parameters measured in the normotensive subjects during treatment with prazosin revealed significant changes. 3. Sub-classification of the hypertensive patients into low-, normal- and high-renin categories revealed significant decreases of renin in all six patients with high renin- and in four out of 12 patients with normal renin- but not in the two patients with low renin-essential hypertension. 4. The results indicate that prazosin exerts its hypotensive action and suppresses plasma renin activity particularly in patients with high renin-essential hypertension. These may be considered to have increased sympathetic drive. 5. Conceivably, the blood pressure-lowering effect of prazosin is effected by peripheral vasodilatation and also by a decreased venous return to the heart.

1976 ◽  
Vol 51 (s3) ◽  
pp. 177s-180s ◽  
Author(s):  
R. Gordon ◽  
Freda Doran ◽  
M. Thomas ◽  
Frances Thomas ◽  
P. Cheras

1. As experimental models of reduced nephron population in man, (a) twelve men aged 15–32 years who had one kidney removed 1–13 years previously and (b) fourteen normotensive men aged 70–90 years were studied. Results were compared with those in eighteen normotensive men aged 18–28 years and eleven men aged 19–33 years with essential hypertension. 2. While the subjects followed a routine of normal diet and daily activity, measurements were made, after overnight recumbency and in the fasting state, of plasma volume and renin activity on one occasion in hospital and of blood pressure on five to fourteen occasions in the home. Blood pressure was also measured after standing for 2 min and plasma renin activity after 1 h standing, sitting or walking. Twenty-four hour urinary aldosterone excretion was also measured. 3. The measurements were repeated in the normotensive subjects and subjects in (a) and (b) above after 10 days of sodium-restricted diet (40 mmol of sodium/day). 4. The mean plasma renin activity (recumbent) in essential hypertensive subjects was higher than in normotensive subjects. In subjects of (a) and (b) above, it was lower than normotensive subjects, and was not increased by dietary sodium restriction in subjects of (a). 5. The mean aldosterone excretion level was lower in old normotensive subjects than in the other groups, and increased in each group after dietary sodium restriction. 6. Mean plasma volume/surface area was not different between the four groups and in normotensive, essential hypertensive and nephrectomized subjects but not subjects aged 70–90 years was negatively correlated with standing diastolic blood pressure.


1982 ◽  
Vol 12 (1) ◽  
pp. 145
Author(s):  
Soon Kyu Suh ◽  
Sae Wha Yoo ◽  
Soon Chang Park ◽  
Joon Sock Kim ◽  
Kyung Ho Kang ◽  
...  

1982 ◽  
Vol 46 (9) ◽  
pp. 954-963 ◽  
Author(s):  
YASUHIRO NODA ◽  
KOSHIRO FUKIYAMA ◽  
KENSHI KUMAMOTO ◽  
SHUICHI TAKISHITA ◽  
TERUKAZU KAWASAKI ◽  
...  

1978 ◽  
Vol 55 (s4) ◽  
pp. 367s-371s ◽  
Author(s):  
G. Bianchi ◽  
G. B. Picotti ◽  
G. Bracchi ◽  
D. Cusi ◽  
M. Gatti ◽  
...  

1. Almost all the factors that may cause a rise in blood pressure are, in turn, influenced by the increase in blood pressure per se. Thus any primary involvement of one or more of these factors in the pathogenesis of essential hypertension must be evaluated before or during the development of hypertension. 2. Young normotensive subjects both of whose parents are hypertensive have a much higher probability of developing hypertension than those whose parents are both normotensive. 3. The following measurements were made in 56 subjects of the first group (both parents hypertensive) and 35 of the second group (both parents normotensive), matched for age, sex and body surface area: renal plasma flow and glomerular filtration rate, using p-aminohippurate and inulin clearance; 24 h urinary excretion of aldosterone, protein and electrolytes; plasma renin activity; plasma volume. Plasma catecholamines and cardiac index were also measured in 26 subjects of the first group and 25 subjects of the second group using a radioenzymic method and echocardiography. 4. All these factors were similar in the two groups except that renal plasma flow was higher in the first group (767·2 ± 30 versus 650·7 ± 17 ml/min, P < 0·01). Plasma renin activity tended to be lower in subjects with a higher renal plasma flow, but there was no significant negative correlation between the two factors. 5. The possibility that the higher renal plasma flow in subjects with a high probability of developing hypertension is a compensatory mechanism for a primary intrarenal defect is discussed.


1977 ◽  
Vol 53 (1) ◽  
pp. 87-91 ◽  
Author(s):  
M. H. Snow ◽  
D. A. Piercy ◽  
Valerie Robson ◽  
R. Wilkinson

1. In 29 patients with acromegaly, plasma renin activity and growth hormone were measured during fasting and recumbency on free diet. Exchangeable sodium was measured in all cases and expressed as a percentage of the expected value on the basis of lean body mass. 2. Twenty-two control subjects without evidence of cardiovascular, renal or endocrine disease were studied in the same way. 3. There was a significant increase in exchangeable sodium and suppression of plasma renin activity in the acromegalic patients in comparison with control subjects. 4. There was a significant positive correlation between exchangeable sodium and plasma growth hormone. 5. Hypertensive acromegalic patients (diastolic blood pressure ≥ 100 mmHg) tend to have a lower (although not significantly so) exchangeable sodium than normotensive subjects. 6. We conclude that (a) suppression of plasma renin activity in acromegaly can be explained by sodium retention, (b) hypersecretion of growth hormone is probably responsible for the increased exchangeable sodium, and (c) sodium overload cannot be directly related to blood pressure but may contribute to the increased occurrence of hypertension in acromegaly.


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