Why the study?
Does the atriopeptidase inhibitor UK 69,578 increase endogenous ANF and cause natriuresis in normal volunteers?
Does the atriopeptidase inhibitor UK 69,578 increase endogenous ANF and cause natriuresis in normal volunteers?
Inhibition of atriopeptidase with UK 69,578 elevates endogenous ANF and promotes natriuresis in normal humans, suggesting a potential therapeutic mechanism for hypertension and heart failure.
Supports atriopeptidase inhibition for hypertension and heart failure; extends ANF-natriuresis proof-of-concept to humans.
The endopeptidase EC 3.4.24.11 (atriopeptidase) degrades atrial natriuretic factor (ANF). Intravenous administration of UK 69,578 (0.025 to 10.0 mg/kg), a new specific atriopeptidase inhibitor, in 16 normal volunteers produced a two- to three-fold rise in endogenous ANF. Peak levels were reached within 2 h declining to control values by 8 h. The rise in ANF was associated with an increase in urine volume and mean urinary sodium excretion rose from 64.9 mmoles/8 h after placebo to 116.1 mmoles/8 h after 10 mg/kg UK 69,578. Despite the natriuresis, plasma active renin concentration was suppressed for up to 8 h. We conclude that inhibition of the endopeptidase EC 3.4.24.11 in humans elevates endogenous ANF and causes a natriuresis and may offer a novel therapeutic approach to the treatment of hypertension and cardiac failure.
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Jardine et al. (1990) studied this question.
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