Studies on renomedullary prostaglandin and renal kallikrein-kinin system in hypertension.

Abstract

Urinary excretion of kinin, of kallikrein, of prostaglandin (PG) E and A, of main urinary metabolite (MUM) of PGF₂α and plasma PGE concentration were measured in healthy subjects and in hypertensive patients. The kallikrein excretion rates were 111 ± 11.0 (SE) KU/day in 21 normal subjects, 75 ± 10 KU/day in 23 patients with essential hypertensives and 175 ± 23 KU/day in 9 patients with primary aldosteronism. The kallikrein output in urine was decreased in essential hypertension, while increased in primary aldosteronism. The excretion rates of urinary kinin were increased in primary aldosteronism. The excretion rates of urinary kinin were 44.8 ± 5.9 μg/day in 24 normal subjects and 21.7 ± 4.7 μg/day in 19 patients with essential hypertension. The urinary kinin excretion was also decreased in essential hypertension. The PGE and A excretion rates were 482 ± 5.5 ng/day in 17 normal subjects and 321 ±44 ng/day in 26 patients with essential hypertension. The urinary output of PGE and A was decreased in essential hypertension. Regarding the output of PGF₂α-MUM or plasma PGE concentration, there was no significant difference between normal subjects and essential hypertension. Influences of furosemide on urinary kallikrein and PGE were examined. Enhancement of urinary excretion of kallikrein and PGE were found in normal subjects and in essential hypertension after the administration of furosemide. The percent increases of urinary kallikrein output were 489% in normal subjects and 312% in essential hypertension, and urinary PGE output were 518% in the former and 143% in the latter. In essential hypertension the increase was smaller than in healthy subjects. The present experiment proved a decrease in synthesis of renal kallikrein, kinin, and PGE in essential hypertension, suggesting that suppression of renal depressor system is one of the etiological factors in essential hypertension.