ACUTE HYPERTENSION IMPAIRS ENDOTHELIUM-DEPENDENT VASODILATATION

1. Previous investigations have demonstrated an impaired endothelium-d ependent vasodilatation (EDV) in patients with hypertension. The prese nt study aimed to investigate if an acute rise in blood pressure to hy pertensive levels impairs EDV in otherwise normotensive subjects. 2. T wenty-seven young, healthy, normotensive subjects were studied. Eight of these underwent evaluation of EDV and endothelium-independent vasod ilatation (EIDV) by means of forearm blood flow measurements during lo cal intra-arterial infusions of methacholine (2 and 4 mu g/min) and so dium nitroprusside (5 and 10 mu g/min), before and after 1 h of sustai ned hypertension, induced by noradrenaline given intravenously. Identi cal measurements were made in 11 subjects before and during concomitan t local intra-arterial infusion of noradrenaline without change in blo od pressure and eight subjects were studied during saline infusions. 3 . One hour of sustained hypertension (diastolic blood pressure >95 mmH g) significantly attenuated both forearm blood flow (17.4 +/- 6.8 vers us 27.4 +/- 6.8 ml . min(-1) . 100 ml(-1) tissue at baseline, P < 0.05 ) and forearm vascular resistance decrease (3.2 +/- 0.87 versus 7.4 +/ - 2.5 units at baseline, P < 0.05) during methacholine infusion. These attenuations were significantly more pronounced for methacholine than for sodium nitroprusside (P < 0,05), In contrast, local intra-arteria l noradrenaline infusions impaired vasodilatation induced by methachol ine and sodium nitroprusside to a similar extent. Saline infusions did not change either EDV or EIDV, 4.Thus, an acute rise in blood pressur e to hypertensive levels induced by noradrenaline impaired EDV more th an EIDV in otherwise normotensive subjects, while no such selective ef fect of local noradrenaline was seen, suggesting that a high blood pre ssure impairs endothelial vasodilator function.