Enhanced blood pressure increase after prostaglandins synthesis inhibition in the early phase of renal hypertension; an opposing role for the contralateral kidney.

Application of a solid renal artery clip (0.25 mm i.d.) in rats with an undisturbed contralateral kidney (two-kidney one clip renal hypertension; 2KH ) causes a small increase in blood pressure within the first 3 hr. After pretreatment of the animals with aspirin the blood pressure response was enhanced. In contrast, in unilaterally nephrectomized rats after clipping(one-kidney one clip renal hypertension; 1KH ), the increase in blood pressure of the control and aspirin pretreated group was similar and at the level of the aspirin pretreated group of the 2KH -rats. One day after clipping in the 2KH -rats there was still a marked enhancement of the blood pressure increase induced by the prostaglandin-synthesis inhibitor. Plasma renin activity of the aspirin and control group 1 hr after clipping was significantly increased as compared to the sham operated animals in as well the 2KH - and 1KH -rats. The converting enzyme inhibitor captopril attenuates the acute increase in blood pressure in both control and aspirin treated 2KH - and 1KH -rats pointing to a major role for angiotensin II. It is suggested that the potentiation of blood pressure after prostaglandin synthesis inhibition is due to a diminished release of prostaglandins by the contralateral kidney. The data indicate that in intact rats prostaglandins may act as breaking mechanism against hypertensive influences such as a sudden increase in blood pressure by angiotensin II.