Extent of baroreceptor resetting in response to sodium nitroprusside and verapamil.

We investigated the effect of sodium nitroprusside, verapamil, and hemorrhage on the resetting of the aortic baroreceptors of normotensive control rats to hypotension, and the reversal of resetting of baroreceptors of one-kidney, one clip hypertensive rats to normotension. Using whole-nerve recording, the extent (%) of resetting (or reversal of resetting) observed 15 minutes after a maintained fall in mean arterial pressure (MAP) was evaluated by the ratio between changes of systolic threshold pressure for baroreceptor activation and changes of control diastolic pressure exhibited by the rats, multiplied by 100. Three groups of normotensive control rats showed a MAP decrease to hypotensive levels of 33%, 39%, and 41%, respectively, with sodium nitroprusside, verapamil, and hemorrhage. The corresponding extent of resetting was 96 +/- 3%, 39 +/- 2%, and 46 +/- 4%, respectively. Only in the group treated with verapamil did MAP and systolic threshold pressure not revert completely to normotensive levels 15 minutes after the end of drug infusion. Three groups of one-kidney, one clip hypertensive rats showed MAP normalization of 30%, 37%, and 31%, respectively, with sodium nitroprusside, verapamil, and hemorrhage. The corresponding extent of reversal of resetting to normotension was 107 +/- 3%, 40 +/- 2%, and 60 +/- 9%, respectively. Again, only in the group treated with verapamil did MAP and systolic threshold pressure not revert to hypertensive levels 15 minutes after infusion. Besides indicating that different vasodilators can differently modulate the rapid (15-minute) resetting (or reversal of the resetting) due to similarly maintained fall in MAP, these data suggest that verapamil has a nonspecific effect on the baroreceptors, whereas sodium nitroprusside appears to affect baroreceptor transduction.