ABSTRACT
It is increasingly recognized that the endothelium plays an important role in the control of vascular tone by releasing both vasodilating and vasoconstricting substances (Furchtgott and Zawadsky, 1980; Yanagisawa et al., 1988; Vanhoutte, 1989; Vane et al., 1990). These mechanisms are important both for the regulation of microvascular (Linder et al., 1990; Kiowski et al., 1991; Panza et al., 1993; Haynes and Webb, 1994) and larger conduit arteries (Joannides et al., 1995; Hornig et al., 1996). Patients with chronic heart failure are hemodynamically characterized by increased vasoconstriction and a reduced vasodilator response to exercise (Zelis et al., 1968). These abnormalities appear to be due to a number of compensatory mechanisms and some neurohumoral factors involved in this impaired vasodilator response have been studied extensively in the past. However, there is growing evidence now to suggest that the endothelium also plays an important role in the abnormal vasodilator response. In particular, the role of endothelium-derived nitric oxide has received considerable attention. The present review, therefore, summarizes the evidence for a reduced vasodilator capacity of the endothelium in chronic heart failure and focuses on the potential mechanisms underlying this abnormality. In addition, the importance of endothelial vasoconstrictor mechanisms is also discussed.
