Hypertension is one of the conditions in which the clinical syndrome of 'coronary insufficiency with normal coronary angiogram' is most frequently encountered. An alteration in the endothelium-dependent vasomotility of coronary circulation as a result of a reduced nitric oxide bioavailability or of the production of endothelium-dependent contracting factors could be a mechanism of this syndrome. There is no specific information available concerning the possibility that hypertension by itself reduces basal nitric oxide activity in coronary circulation. In contrast, several data indicate the presence of agonist-induced endothelial dysfunction in the coronary microcirculation of essential hypertensive patients. However, these data are contradictory in hypertensive patients without left ventricular hypertrophy. The same studies reported no difference in the vasodilating response to acetylcholine between normotensive and hypertensive patients, while other studies showed that the increase in coronary blood flow induced by acetylcholine was significantly less in hypertensive patients than in normotensive control subjects. We showed that in patients with essential hypertension without any other cardiovascular risk factors and with angiographically normal coronary arteries, endothelium-dependent vasomotion is heterogeneous, since only one half of the patients shows a reduced vasodilation or a paradoxical vasoconstriction to acetylcholine. This endothelial dysfunction seems to be caused by a reduction in agonist-induced nitric oxide production and, in some hypertensive patients with more marked endothelial dysfunction, also by the production of cyclooxygenase-dependent endothelium-dependent contracting factors. Finally, although endothelial dysfunction of coronary microcirculation can cause or contribute to the reduction in coronary reserve, its clinical significance and role in the coronary risk of essential hypertensive patients is still to be established.
Endothelial function and coronary microcirculation in essential hypertension.
TADDEI, STEFANO;VIRDIS, AGOSTINO;GHIADONI, LORENZO;SALVETTI, ANTONIO
1998-01-01
Abstract
Hypertension is one of the conditions in which the clinical syndrome of 'coronary insufficiency with normal coronary angiogram' is most frequently encountered. An alteration in the endothelium-dependent vasomotility of coronary circulation as a result of a reduced nitric oxide bioavailability or of the production of endothelium-dependent contracting factors could be a mechanism of this syndrome. There is no specific information available concerning the possibility that hypertension by itself reduces basal nitric oxide activity in coronary circulation. In contrast, several data indicate the presence of agonist-induced endothelial dysfunction in the coronary microcirculation of essential hypertensive patients. However, these data are contradictory in hypertensive patients without left ventricular hypertrophy. The same studies reported no difference in the vasodilating response to acetylcholine between normotensive and hypertensive patients, while other studies showed that the increase in coronary blood flow induced by acetylcholine was significantly less in hypertensive patients than in normotensive control subjects. We showed that in patients with essential hypertension without any other cardiovascular risk factors and with angiographically normal coronary arteries, endothelium-dependent vasomotion is heterogeneous, since only one half of the patients shows a reduced vasodilation or a paradoxical vasoconstriction to acetylcholine. This endothelial dysfunction seems to be caused by a reduction in agonist-induced nitric oxide production and, in some hypertensive patients with more marked endothelial dysfunction, also by the production of cyclooxygenase-dependent endothelium-dependent contracting factors. Finally, although endothelial dysfunction of coronary microcirculation can cause or contribute to the reduction in coronary reserve, its clinical significance and role in the coronary risk of essential hypertensive patients is still to be established.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
