Effects of intravenous administration of a calcium antagonist on prostaglandins and thromboxane in plasma and urine in humans

Abstract

The effects of a calcium antagonist [Nicardipine hydrochloride (NH)] on the prostaglandin [prostaglandin E2 (PGE2), and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha)] and thromboxane B2 levels in the blood and urine were examined in 6 patients with essential hypertension following intravenous infusion of NH for 120 minutes. At the same time, the plasma renin activity (PRA), plasma aldosterone concentration (PAC), and plasma and urinary electrolyte levels were also determined. During NH administration, the blood pressure was significantly decreased (p less than 0.05) with an increased pulse rate (p less than 0.05). PRA was significantly increased after NH loading (p less than 0.05) but PAC showed no change. The plasma PGE2 and 6-keto-PGF1 alpha levels tended to increase slightly, while the blood thromboxane B2 level showed a decreasing tendency. The 6-keto-PGF1 alpha to thromboxane B2 ratio was significantly increased after NH loading as compared to the preloading ratio (p less than 0.05), and then returned to the preloading value at about 30 minutes after discontinuation of NH loading. The urinary excretions of PGE2, 6-keto-PGF1 alpha and thromboxane B2, PGE2 and 6-keto-PGF1 alpha tended to decrease after NH loading. In particular, the decrease in PGE2 was statistically significant (p less than 0.05). No change occurred in the urinary excretion of thromboxane B2. The above findings indicate that NH increased the plasma 6-keto-PGF1 alpha to thromboxane B2 ratio but decreased the urinary excretion of prostaglandins. In addition, the possible involvement of an enhanced 6-keto-PGF1 alpha/thromboxane B2 ratio in part of the hypotensive mechanism of NH is suggested.