Decreased endothelium-dependent relaxation in New Zealand genetic hypertensive rats.

The relaxation response to endothelium-dependent (acetylcholine and the calcium ionophore A23187) and independent (sodium nitroprusside) vasodilators was examined in isolated aortic ring segments from age-matched genetically hypertensive (GH) and normotensive (N) rats (New Zealand strain). Tissues were initially contracted with methoxamine to achieve similar levels of contractile force. The IC20, IC40 and IC50 values for acetylcholine, A23187 and sodium nitroprusside were shifted significantly to the right (P less than 0.05) in aortic rings from GH rats compared to the corresponding values in N rats. The maximal relaxation achieved by acetylcholine and A23187 was significantly depressed in aortas from GH rats (P less than 0.05). Sodium nitroprusside elicited the maximal relaxation in both groups of tissues. These results demonstrate that there exists a generalized defect in the relaxant ability of vascular smooth muscle from GH rats. In addition, our findings suggest that this defect is coupled with a decreased responsiveness to endothelium-dependent vasodilators in this particular animal model of hypertension.