Renal Hypertensive Rats

Increased blood pressure responsiveness to bradykinin in comparison with other vasodilator agents was demonstrated in rats with long-term one-kidney and two-kidney, one clip hypertension. In the present study, we analyzed the reactivity to intra-aortically injected bradykinin in unanesthetized one-kidney, one clip hypertensive rats during the control period and 1, 5, and 8 hours after reversal of hypertension after removal of the renal artery constriction. One and 5 hours after unclipping the renal artery, the mean blood pressure decreased markedly (from 195±7 to 124±8 and 145±9 mm Hg, respectively), whereas the hyperreactivity to bradykinin reverted only slightly, and the responses to nitroprusside remained unchanged. In another group of hypertensive rats examined 8 hours after unclipping (pressure decreased from 192 ±4 to 143±8 mm Hg), the hyperreactivity to bradykinin had partially reverted. Significantly larger doses of bradykinin were necessary to produce the same decrease in blood pressure when compared with the control period (16.4±2.0 vs. 7.2±1.2 ng). The same degree of reversal of hyperreactivity to bradykinin was observed when the blood pressure of hypertensive rats was reduced (from 207±8 to 143±5 mm Hg) during 1 hour by hydralazine injection. Complete reversibility of bradykinin hyperreactivity was produced by nitroprusside infusion (from 201 ±13 to 142±10 mm Hg). Pronounced enhancement of the blood pressure reactivity to bradykinin was observed in normotensive rats submitted to acute hypertension (15 minutes) produced by phenylephrine infusion (from 131±2 to 193±3 mm Hg) and a fivefold decrease in bradykinin reactivity was produced after 1 hour of hypotension (from 128±4 to 91 ±3 mm Hg) by hydralazine infusion. The data suggest that blood pressure responsiveness to bradykinin is markedly affected by the level of pressure, probably because of the degree of vasoconstriction and vasodilation existing in the rats. (Hypertension 1990;15(suppl I):I-140-I-143)