The Effects of Captopril on the Acute Vascular Responses to Frusemide in Man

Abstract

To examine the importance of angiotensin II formation in the production of frusemide's acute peripheral venous and arterial responses, the effect of pretreatment with captopril was studied. Captopril abolished the acute increases in venous capacitance and blood pressure and attenuated the increases in forearm vascular resistance produced by intravenous frusemide. The study provides evidence that angiotensin II formation performs an essential role in the production of the acute vascular effects of frusemide in man.

Inhibition of vasoconstriction by frusemide in the rat

“…Intra-renal angiotensin II may then mediate the prostaglandin production as it is known that angiotensin II can release arachidonic acid and prostaglandins (Gryglewski et al, 1980). Recently the increase in venous capacitance seen in man after frusemide has been suggested to be prostaglandin-mediated but secondary to the production of renin and angiotensin II from the kidney by frusemide (Johnston et al, 1983).…”

Frusemide, ACE inhibition, renal dopamine and prostaglandins: acute interactions in normal man.

“…Blood pressure tended to fall with ramipril alone and although not achieving statistical significance this may have modified the hormonal and haemodynamic response to frusemide. Johnston et al (1983) and have shown that an acute rise in blood pressure occurs immediately following frusemide injection which is abolished by ACE inhibition. In this study we have found a similar although non-significant rise after frusemide but the ACE treated group also showed a trend to rise.…”

“…In this study we have found a similar although non-significant rise after frusemide but the ACE treated group also showed a trend to rise. Johnston et al (1983) used subjects taking a low salt intake and gave a relatively large dose of ACE inhibitor which caused a significant fall in blood pressure. Our subjects had a much higher salt intake and our dose of ACE inhibitor was relatively small and these factors may account for the differences.…”

The effects of propranolol and digoxin on the acute vascular responses to frusemide in normal man.

“…The study was carried out at the same time of day on three separate occasions with a period of at least 1 week between studies. For the 3 days before each part of the experiment, subjects received 60 mmol of sodium daily in their diet and 80 mg of oral frusemide daily (Johnston et al, 1983b (Whitney, 1953 After a 1 h period of rest in the supine position, three baseline measurements of venous capacitance, forearm blood flow, blood pressure and heart rate were made at 5 min intervals and a blood sample taken for measurement of plasma renin activity and plasma aldosterone concentrations. Subjects then received 750 ,ug digoxin, 10 mg propranolol (dissolved in 20 ml normal saline) or 20 ml normal saline delivered at a rate of 1 ml min-' according to a doubleblind, randomised cross-over design.…”