DIFFERENTIAL CONTRIBUTION OF ENDOTHELIAL FUNCTION TO VASCULAR REACTIVITY IN CONDUIT AND RESISTANCE ARTERIES FROM DEOXYCORTICOSTERONE-SALT HYPERTENSIVE RATS

The purpose of these studies was to compare changes in conduit and res istance artery function in deoxycorticosterone-salt hypertensive rats. We hypothesized that if there was a common mechanism producing change s in vascular function in hypertension then there would be similar alt erations in reactivity of conduit and resistance arteries. Helically c ut strips of common carotid artery were prepared for measurement of is ometric force generation, and segments of small mesenteric arteries we re pressurized for video dimension analysis. Sensitivity of arteries t o phenylephrine and acetylcholine was determined. Carotid arteries fro m deoxycorticosterone-salt hypertensive rats were more sensitive to ph enylephrine than arteries from control rats, whereas mesenteric resist ance arteries from hypertensive rats were less sensitive to phenylephr ine. In carotid arteries, endothelial denudation or incubation with N- omega-nitro-L-arginine increased phenylephrine sensitivity in control rats to the level seen in deoxycorticosterone-salt rats. These manipul ations had no effect on phenylephrine sensitivity in arteries from deo xycorticosterone-salt rats. In mesenteric resistance arteries, endothe lium denudation normalized the depressed phenylephrine sensitivity in arteries from hypertensive rats but had no effect on arteries from nor motensive rats. This depressed phenylephrine sensitivity in deoxycorti costerone-salt mesenteric arteries was not reversed by incubation with N-omega-nitro-L-arginine. Acetylcholine-induced relaxation was depres sed in carotid arteries from deoxycorticosterone-salt hypertensive rat s, and N-omega-nitro-L-arginine blocked these relaxations. In contrast , acetylcholine relaxation in the mesenteric arteries from normotensiv e and hypertensive rats did not differ. N-omega-nitro-L-arginine sligh tly but significantly attenuated acetylcholine dilation only in mesent eric resistance arteries from the hypertensive rats. We conclude that qualitatively different changes in vasoconstrictor sensitivity to phen ylephrine occur in carotid arteries and mesenteric resistance arteries of deoxycorticosterone-salt hypertensive rats. The increased phenylep hrine sensitivity in carotid arteries in this model of hypertension is due to the loss of endothelium-derived nitric oxide production. In co ntrast, the decreased phenylephrine sensitivity in mesenteric resistan ce arteries from deoxycorticosterone-salt rats is due to a non-nitric oxide-mediated influence of the endothelium that is absent in arteries from normotensive rats.