1980 Volume 27 Issue 6 Pages 769-773
5α-dihydrocortisol has been reported to amplify the mineralocorticoid activity of aldosterone. In this study 5α-dihydrocortisol was administered to unilaterally nephrectomized rats treated with 11-deoxcorticosterone acetate (DOCA) and sodium chloride to examine its potentiating effect on the elevation of blood pressure in these animals. Subcutaneous administration of DOCA at two dose levels (40μg and 100μg/100g of body weight 3 times a week) resulted in a significant rise in blood pressure when compared with controls given no DOCA. However, concomitaut injection of 5α-dihydrocortisol (300μg/100 g of body weight 3 times a week) with both doses of DOCA did not accelerate the development or potentiate the severity of the hypertension in a 4 week period. Furthermore, administration of 5α-dihydrocorlisol did not cause a further decrease in plasma renin activity or a greater increase in urinary kallikrein excretion than those observed after DOCA alone. Thus, 5α-dihydrocortisol does not potentiate DOCA in the production of low renin hypertension in unilaterally nephrectomized salt-loaded rats.
