Abstract
Arterial hypertension represents a major risk factor for cardiovascular morbidity and mortality: increasing experimental and clinical evidence suggest that a major role can be played by myocardial ischemia. A reduction of coronary vasodilator reserve, i.e. the capability of coronary system to increase flow in response to an increased metabolic demand, has been reported in several models of animal and human hypertension even in absence of angiographically detectable coronary atherosclerosis (1–4).
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