PRESERVED ENDOTHELIUM-DEPENDENT VASODILATATION IN PATIENTS WITH ESSENTIAL-HYPERTENSION

Background. Previous studies suggest that vascular endothelial functio n may be impaired in essential hypertension. Although muscarinic agoni sts dilate blood vessels by releasing an endothelium-derived relaxing factor closely related to nitric oxide, nitroprusside dilates vessels by a mechanism that is independent of the endothelium. The finding of an impaired response to muscarinic agonists but a normal response to n itroprusside in patients with hypertension has suggested that endothel ial function is abnormal in hypertension. Methods. We reassessed this issue by measuring forearm blood flow by plethysmography during the in fusion of vasodilators into the brachial arteries of 95 subjects: 37 n ormotensive controls (mean [+/-SE] arterial blood pressure, 92+/-1 mm Hg) and 58 patients with essential hypertension (mean arterial blood p ressure, 121+/-1 mm Hg). Results. In an initial study, vascular respon ses to the vasodilators carbachol and nitroprusside were similar in no rmotensive controls (n = 19) and hypertensive patients (n = 17). We wo ndered whether this might be attributable to the use of previously unt reated patients or to the choice of carbachol as the muscarinic agonis t. However, we found that the vasodilator responses to nitroprusside, acetylcholine, carbachol, and isoproterenol were also similar in separ ate groups of normotensive controls (n = 18) and hypertensive subjects , whether the subjects had never been treated for hypertension (n = 24 ) or had had therapy withheld for two weeks (n = 17). The 95 percent c onfidence intervals for the difference between the controls and hypert ensive patients in the ratio of endothelium-dependent vasodilatation i nduced by acetylcholine or carbachol to endothelium-independent vasodi latation induced by nitroprusside were -14 to +23 percent for acetylch oline and -13 to +12 percent for carbachol. Conclusions. In contrast t o previous studies, our findings suggest that selective impairment of the responsiveness of the forearm vasculature to muscarinic agonists i s not universal in patients with essential hypertension.