Author + information
- Received November 16, 1987
- Revision received March 28, 1988
- Accepted April 19, 1988
- Published online January 1, 1988.
- Tudor M. Griffith, MA, MB, BCh, MRCP, FRCR,
- Malcolm J. Lewis, MB, PhD,
- Andrew C. Newby, MA, PhD and
- Andrew H. Henderson, MB, FRCP∗∗
- ↵∗Address for reprints: Andrew H. Henderson, MB, Department of Cardilology, University of Wales College of Medicine, Heath Park, Cardiff, United Kingdom.
This article reviews what is known of endothelium-derived relaxing factor and its possible physiologic and pathophysiologic roles. This relaxing factor is now thought to be nitric oxide or a ready source of it. It acts as an endogenous nitrovasodilator, stimulating soluble guanvlate cyclase to increase cyclic guanosine monophosphate (GMP) levels in vascular smooth muscle and platelets, with consequent relaxant and anti-aggregatory effects (predominantly when stimulated through receptor-operated channels). Its actions are thus synergistic with those of cyclic adenosine monophosphate (AMP)-mediated stimulation (for example, adenosine, prostacyelin).
Endothelium-derived relaxing factor is unstable and is thought lo act only very locally in vivo. Its release is continuous in the basal state and is stimulated by a number of neuropeptides and by agents released during platelet activation and thrombosis—with large differences in activity among different vessels. Endothelium-derived relaxing factor activity is also flow related, thereby coordinating vasomotor behavior in an intact vascular tree in response to changes in flow. Endothelium-derived relaxing factor activity is reduced in several pathologic states, including atherosclerosis.
- Received November 16, 1987.
- Revision received March 28, 1988.
- Accepted April 19, 1988.
- American College of Cardiology