Role of renal thromboxane in salt-sensitive blood pressure rise in DOCA salt hypertension

Abstract

Urinary excretion and release of prostaglandins (PG) from isolated glomeruli and renal papilla of deoxycorticosterone acetate (DOCA)-treated rats fed with a normal salt (0.6% NaCl) diet and a high salt (4%NaCl) diet were determined. Mean blood pressure was significantly higher in the high salt diet group than in the normal salt diet group (146.2 +/- 2.3 vs 118.6 +/- 1.9 mmHg, p < 0.01). Urinary excretion of thromboxane (Tx) B2, stable metabolite of Tx A2, and 6-keto PG-F1 alpha, a stable metabolite of prostacyclin, increased significantly in the high salt diet group compared to the values of the normal salt diet group increased significantly by 104%, 55%, and 74% compared to those of the normal salt diet group, respectively. Release of 6-keto-PG F1 alpha from renal papilla of the high salt diet group decreased significantly, but there were no intergroup differences in the release of PG E2 and Tx B2. Stepwise multiple linear regression analysis showed that the significant contributory factors underlying the mean blood pressure were urinary excretion of Na (F = 14.187, p < 0.01) and release of Tx B2 from isolated glomeruli (F = 4.135, p < 0.05). These findings suggest that the manifestation of Tx synthesis in renal glomeruli has a predominant role in the salt sensitive pressor response of DOCA salt hypertension in rats.