Acute effects of a new vasodilator, Ro 12-4713, on blood pressure, plasma renin activity, aldosterone and catecholamine levels, and renal function in hypertensive and normal subjects

1981 ◽  
Vol 20 (3) ◽  
pp. 169-177 ◽  
Author(s):  
M. Grimm ◽  
P. Weidmann ◽  
A. Meier ◽  
W. H. Ziegler ◽  
F. C. Reubi
1985 ◽  
Vol 69 (2) ◽  
pp. 239-240 ◽  
Author(s):  
Sergio De Marchi ◽  
Emanuela Cecchin

We are very interested to read the paper by Bannan et al. [1] about the effect of alcohol withdrawal on blood pressure, plasma renin activity, aldosterone, cortisol and dopamine β-hydroxylase. It has been known for several years that alcoholic patients admitted to hospital for detoxification have a high prevalence of hypertension [2]. Their blood pressures return to normal after alcohol withdrawal symptoms have abated and they remain normal if they continue to abstain. Patients who resume drinking sustain a rise in blood pressure to their former high levels.


1981 ◽  
Vol 60 (4) ◽  
pp. 399-404 ◽  
Author(s):  
C. J. Mathias ◽  
H. L. Frankel ◽  
I. B. Davies ◽  
V. H. T. James ◽  
W. S. Peart

1. The effect of endogenous sympathetic stimulation (induced by urinary bladder stimulation) and intravenous infusion of noradrenaline and isoprenaline on blood pressure, heart rate and levels of plasma renin activity and plasma aldosterone were studied in six tetraplegic patients. Data from infusion studies were compared with data from six normal subjects studied in an identical manner. 2. Bladder stimulation in the tetraplegic patients caused a marked rise in blood pressure and fall in heart rate, but no change in plasma renin activity or plasma aldosterone. 3. Noradrenaline infusion resulted in an enhanced pressor response in the tetraplegic patients when compared with the normal subjects. Heart rate fell in both groups. Plasma renin activity and plasma aldosterone did not change in either group. 4. Isoprenaline infusion caused a fall in both systolic and diastolic blood pressure in the tetraplegic patients, unlike the normal subjects in whom there was a rise in systolic and a fall in diastolic blood pressure. Heart rate and plasma renin activity rose in both groups. Plasma aldosterone did not change in either group. 5. We conclude that in tetraplegic patients neither endogenous sympathetic stimulation by bladder stimulation nor infusion of noradrenaline raises plasma renin activity. Isoprenaline increases plasma renin activity to the same extent as in normal subjects. Renin release mechanisms in tetraplegic patients therefore do not appear to be hypersensitive to catecholamines. Plasma aldosterone is not influenced by any of the stimuli.


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