GLOMERULAR THROMBOXANE CONTRIBUTES TO PRESSOR-RESPONSE IN DEOXYCORTICOSTERONE ACETATE-SALT HYPERTENSION

To assess the role of renal thromboxane in a salt sensitive presser re sponse in hypertension, urinary excretion of thromboxane and its relea se from isolated glomeruli and renal papillae were examined in deoxyco rticosterone acetate treated rats with normal (0.6%, n = 12) and high (4%, n = 12) salt diets for 8 weeks. Mean blood pressure, measured dir ectly by an implanted aortic catheter, was higher in the high salt die t group than in the normal salt diet group (146 +/- 2 vs 119 +/- 2 mmH g, P< 0.01). Urinary excretion of thromboxane B-2 and 6-keto-prostagla ndin F-1 alpha in the high salt group were significantly higher than t hose in the normal salt diet group, but there was no difference in uri nary excretion of prostaglandin E-2 between the two groups. Release of thromboxane B-2, 6-keto-prostaglandin F-1 alpha, and prostaglandin E- 2 from isolated glomeruli in the high salt diet group increased signif icantly by 104%, 55%, and 74%, respectively, compared with the normal salt diet group. Stepwise multiple linear regression analysis showed t hat significant contributory factors for mean blood pressure in deoxyc orticosterone acetate treated rats were urinary excretion of sodium (F =14.187, P< 0.01) and release of thromboxane B-2 from isolated glomeru li (F=4.135, P<0.05). The unstandardized coefficient (R) calculated fr om the regression function using these two factors was 0.875 and R-2 w as 0.765. The manifest synthesis of thromboxane in renal glomeruli has an important role on salt sensitive presser response in deoxycorticos terone acetate-salt hypertension of rats.