Effects of orally administered glandular kallikrein on urinary kallikrein and prostaglandin excretion,plasma immunoreactive prostanoids and platelet aggregation in essential hypertension

Summary The effects of orally administered glandular kallikrein on urinary kallikrein, aldosterone and prostaglandin E (PGE) excretion, plasma renin activity (PRA), immunoreactive 6-keto PGF₁ and thromboxane B₂ concentrations and platelet aggregation were studied in 12 patients with essential hypertension (EH). After a 2-week control period, each patient was given orally 450 KU/day of hog glandular kallikrein for 8 weeks. Urinary kallikrein, aldosterone and PGE excretion, and plasma 6-keto PGF₁ and thromboxane B₂ concentrations were measured by radio-immunoassay. Platelet aggregation was measured by the addition of ADP, collagen or ristocetin with an aggregometer. Urinary kallikrein excretion and plasma 6-keto PGF₁ concentration were significantly decreased in patients with EH. There were no significant differences in PRA, urinary aldosterone excretion and plasma thromboxane B₂ concentrations between control subjects and patients with EH. There was a significant decrease in blood pressure in patients with EH coinciding with significant increases of urinary kallikrein and PGE excretion and plasma immunoreactive 6-keto PGF₁ concentration after administration of glandular kallikrein. There was also a significant inhibition of platelet aggregation induced by collagen in these patients. Thus, a suppression of the kallikrein-kinin-prostaglandin system in patients with EH was found, and a decrease in blood pressure with an increment of urinary kallikrein, PGE excretion, plasma immunoreactive 6-keto PGF₁ and inhibition of platelet aggregation in vivo by the administration of glandular kallikrein.Abbreviations BK bradikinin - EH essential hypertension - KU kallikrein unit - PG prostaglandin - PRA plasma renin activity - PRP platelet rich plasma - TX thromboxanePresented at IXth European Congress of Cardiology Düsseldorf, July 8–12, 1984