Effect of Oxprenolol on Catecholamines and Plasma Renin Activity: Acute Response to Frusemide in Hypertensive Patients

The role of the sympathetic nervous system in furosemide-induced renin release was investigated in six normal subjects. After intravenous administration of furosemide, plasma renin concentrations increased more than two-fold within 15 min. Neither replacement of urinary fluid loss by intravenous infusion of saline nor pharmacological beta-blockade with d,1-propranolol changed the renin response to furosemide. The activity of the sympathetic nervous system, as estimated by measurement of plasma catecholamine concentrations, remained at the reference level after furosemide. It is concluded that the sympathetic nervous system is not involved in renin release after intravenous administration of furosemide.

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Lack of adrenergic influence on renin release after furosemide in normal man

Elmgreen

Hesse

Christensen

1981

Eur J Clin Pharmacol

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Sequential changes in plasma renin activity and plasma catecholamines in mildly hypertensive patients during acute, furosemide-induced body-fluid loss

Cannella

Galva

Campanini

et al. 1983

Eur J Clin Pharmacol

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To evaluate the role of adrenergic mechanisms in the acute response of renin to furosemide, plasma renin activity (PRA) and plasma catecholamine concentrations were measured for 3 h after i.v. administration of furosemide 1 mg/kg to 8 patients with mild essential hypertension. Furosemide induced a prompt and long-lasting increase in renin, with PRA more than doubled at all times. The increase in PRA within the first 30 min paralleled the peak increases in urinary water and sodium flow rates, and significant decreases in plasma volume and central venous pressure. There was no change in plasma catecholamine concentrations. Plasma noradrenaline was increased significantly at 60 min and adrenaline at 90 min, once furosemide had induced a marked loss of body-fluid and approximately 65% decrease in central venous pressure. Both catecholamines remained elevated until the end of the study, whereas urinary water and sodium flow rates had returned to their pre-treatment values by 150 min. Mean blood pressure was essentially unchanged throughout the study, whereas heart rate increased significantly after 90 min. The findings suggest that in mildly hypertensive patients adrenergic mechanisms are not involved in the initial renin response to furosemide, but they come into play later, probably as a result of reflex sympathetic activation triggered by marked volume depletion.

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Haemodynamic and Hormone Responses to Acute and Chronic Frusemide Therapy in Congestive Heart Failure

et al. 1980

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1. Since important interrelationships between haemodynamic and hormone indices are possible in cardiac failure, measurements of cardiac output, mean pulmonary artery pressure, plasma renin activity, angiotensin II and aldosterone were carried out before and during acute and chronic frusemide therapy in patients with oedematous heart failure who had been given digoxin. 2. Cardiac output fell significantly 90 min after acute frusemide infection, then returned to baseline. Mean pulmonary artery pressure declined steadily throughout the 4 h of observation. 3. These haemodynamic changes occurred in the absence of major hormonal fluctuations and related presumably to direct vascular and diuretic actions of frusemide. 4. With more chronic (8-10 days) oral frusemide therapy, reciprocal changes between haemodynamic and hormone indices were observed. As the diuretic response to frusemide diminished, cardiac output and pulmonary artery pressure declined whereas the renin-angiotensin system was activated. Statistically significant inverse correlations were observed between these haemodynamic and hormone indices. 5. In both acute and chronic phases of the study, fluctuations in aldosterone levels were regulated by the renin-angiotensin system whereas ACTH, plasma potassium and plasma sodium played, at best, supportive roles.

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Effect of Oxprenolol on Catecholamines and Plasma Renin Activity: Acute Response to Frusemide in Hypertensive Patients

Cited by 5 publications

References 7 publications

Lack of adrenergic influence on renin release after furosemide in normal man

Lack of adrenergic influence on renin release after furosemide in normal man

Sequential changes in plasma renin activity and plasma catecholamines in mildly hypertensive patients during acute, furosemide-induced body-fluid loss

Haemodynamic and Hormone Responses to Acute and Chronic Frusemide Therapy in Congestive Heart Failure

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