Coronary endothelial dysfunction in hypertension

: Intracoronary injection of acetylcholine leads to coronary vasodilatation in normal subjects and vasoconstriction in hypertensive subjects, suggesting an abnormality of endothelial function in hypertension. In order to study the response to physiological stimulation which induces endothelium-dependent vasodilatation, the effects of sympathetic stimulation (cold pressor test) and of the increase in flow velocity in the left anterior descending artery were analysed in 10 control and 26 hypertensive subjects. All had angiographically normal coronary arteries and normal lipid profiles. None of the subjects were smokers or diabetic. During the cold test (12 patients), the flow velocity increased by 47 +/- 26% (p < 0.05) in controls and by 68 +/- 48% (p < 0.01) in the hypertensives. Dilatation of the coronary arteries was observed in controls (+12.0 +/- 4.5%, p < 0.001) and constriction in the hypertensives (-10.3 +/- 8.5%, p < 0.001). Injection of papaverine in the distal left anterior descending artery (14 patients) induced proximal dilatation in controls (+17.0 +/- 10.6%, p < 0.001) and was ineffective in hypertensives (-0.4 +/- 1.5%), whereas the flow velocity increased by 521 +/- 129% and 406 +/- 120% (p < 0.001) respectively. Intracoronary injection of 2 mg of isosorbide dinitrate induced comparable dilatation in control subjects (+30.0 +/- 12.9%, p < 0.001) and in the 26 hypertensives (+22.8 +/- 6.5%, p < 0.001). In 10 hypertensive patients, intravenous injection of an angiotensin converting enzyme inhibitor, perindoprilat, immediately re-established the vasodilatory response to these two stimuli. The authors conclude that the coronary responses to physiological stimuli (sympathetic stimulation, increase in flow velocity) are altered in hypertensive subjects with angiographically normal coronary arteries with no other risk factors. Normal vasomotion may be restored by an angiotensin converting enzyme inhibitor.