Why the study?
Does the route of furosemide administration (i.v. vs p.o.) affect the plasma renin activity response in healthy men?
Does the route of furosemide administration (i.v. vs p.o.) affect the plasma renin activity response in healthy men?
The renin response to furosemide differs by route of administration, with oral administration correlating with sodium loss and intravenous administration suggesting alternative mechanisms for early renin hypersecretion.
Answers are grounded in this paper and cite their sources.
Route-dependent PRA kinetics seen in healthy volunteers; leaves open relevance to diuretic response or outcomes in HF.
Plasma renin activity (PRA) was serially determined 0, 15, 30, 60 and 120 min following administration of furosemide in a dose of 40 mg intravenously (i.v.) and 80 mg orally (p.o.) at a one week interval in 10 healthy men. Following i.v. furosemide administration, PRA increased rapidly and reached a plateau level of 6.1 +/- 1.0 ng/ml/h (222 +/- 44% of the control), at 15 min and remained at about the same level throughout the remaining period of the study. In contrast, PRA increased progressively to a maximum level of 5.5 +/- 0.7 ng/ml/h (285 +/- 53% of the control), 120 min after p.o. furosemide. In case of p.o. furosemide, the increase in PRA was dependent on the doses used per body weight, and was significantly correlated with the cumulative sodium excretion by itself, or the cumulative sodium excretion adjusted by either the leanness index or the body surface area. Such relationships were not apparent after i.v. furosemide. These findings suggest that the response of renin release to furosemide in healthy men differs with the routes of administration and renin release with p.o. furosemide may be largely due to a net sodium loss, while mechanism(s) other than sodium loss may be involved in the early hypersecretion of renin with i.v. administration of furosemide.
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Noda et al. (1982) studied this question.
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