Nitric Oxide Activity in the Atherosclerotic Human Coronary Circulation

Abstract

These findings indicate that 1) there is a reduced basal activity of nitric oxide in the human atherosclerotic epicardial and microvascular coronary circulation; and 2) acetylcholine-induced coronary vascular dilation is at least partly due to stimulation of the activity of nitric oxide, and the reduced response to acetylcholine is due to attenuation in the stimulated activity of nitric oxide in patients with atherosclerosis.

Abciximab Attenuates Coronary Microvascular Endothelial Dysfunction After Coronary Stenting

“…18,19 Atherosclerosis impairs coronary endothelium-dependent vasomotion of both conduit and resistance vessels in part because of attenuated NO activity. 20 In the present study, we extend these observations to the immediate post-PCI condition. Because of the ubiquitous need to use nitroglycerin during PCI for the prevention of distal vessel vasospasm, our conclusions are confined to the microvasculature.…”

The endothelial cell in health and disease: its function, dysfunction, measurement and therapy

“…[13][14][15][16]18,21,23,24 Moreover, N G -monomethyl L-arginine (L-NMMA), a NO synthase inhibitor, blunted the vasodilatory response to acetylcholine and FMD, but did not affect nitroprusside-induced vasodilation. 30,31 Endothelial dysfunction contributes to atherosclerosis The NO-cGMP pathway becomes impaired before the development of atherosclerosis and its impairment likely contributes to the pathogenesis of atherosclerosis. In the absence of NO, platelets are better able to adhere, aggregate and release plateletderived growth factor; leukocytes are better able to adhere, promote a chronic inflammatory response and stimulate the growth of underlying cells; more superoxide is available to oxidize LDL; and the vessel is more prone to constriction or 'spasm'.…”

“…Peripheral endothelial function correlates with coronary endothelial function, [36][37][38] 55,56 No test currently fits all these criteria, nor does any test have a universally agreed upon cutoff to define abnormal on the basis of large-scale trials; however, the field is moving toward a test that is simple enough to perform in the office ( Figure 2). Most current tests measure NO-dependent vasodilation, but measuring platelet aggregation and circulating endothelialderived molecules also reflects endothelial function.…”

Coronary artery blood how: Physiologic and pathophysiologic regulation

“…Atherosclerosis causes coronary endothelial dysfunction by significantly reducing NO activity, [113][114] Oxidized low-density lipoproteins (LDL) in the coronary endothelium inhibit the release of L-arginine, the precursor of NO, from endothelial stores, decrease the expression of NO synthase (Fig. 2), and increase the breakdown of NO.115.…”

“…122 Administration of antioxidants such as vitamin E in large doses appears to reduce the oxidation of LDL."' Furthermore, L-arginine supplementation enhances NO production and is reported to reduce intimal thickening in atherosclerotic 113, lZ3, 124 In addition, short-and long-acting nitroglycerin preparations, which are converted into NO, cause venous and arterial dilation by activating guanylate cyclase, increasing cGMP, and thereby producing vascular muscle relaxation (Fig. 2).4O, 120 In this regard, nitroglycerin decreases myocardial oxygen requirements by causing venous dilation and decreasing ventricular preload.…”