Endothelium, coronary vasodilation, and organic nitrates

Am Heart J. 1995 Feb;129(2):382-91. doi: 10.1016/0002-8703(95)90021-7.

Abstract

Recent investigations have suggested that the vascular endothelium is an active participant in the regulation of arterial tone and blood flow. In a state of health, the endothelium contributes to hemodynamic equilibrium; however, it rapidly becomes dysfunctional in hypercholesterolemia and diabetes mellitus or with exposure to the stress of hypertension or long-term smoking. Among the deficits observed during endothelial dysfunction is a reduction in the synthesis and release or an excessive degradation of EDRF. This potent vasorelaxant is derived from the amino acid L-arginine and has been characterized as NO or a closely related substance. EDRF relaxes vascular smooth muscle by activating guanylate cyclase. A deficiency in the activity of EDRF may be the mechanism of diminished coronary vasodilation in patients with ischemic heart disease. Organic nitrates, which are metabolized to NO or S-nitrosothiol at the cellular level, are often used in the management of myocardial ischemia; they also induce vasodilation by activating guanylate cyclase. The similarities between organic nitrates and endogenous EDRF and their interactions are discussed in this review.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Coronary Vessels / drug effects
  • Coronary Vessels / physiology*
  • Endothelium, Vascular / drug effects
  • Endothelium, Vascular / physiology*
  • Humans
  • Myocardial Ischemia / drug therapy
  • Myocardial Ischemia / physiopathology
  • Nitrates / therapeutic use*
  • Nitric Oxide / physiology
  • Vasodilation / drug effects
  • Vasodilation / physiology*

Substances

  • Nitrates
  • Nitric Oxide