The Inhibitory Actions of Anti‐oxidants on Endothelium‐derived Relaxing Factor Released From Cultured Bovine Cells

Read, Mark; Dusting, Gregory J.

doi:10.1111/j.1440-1681.1987.tb00991.x

Cited by 10 publications

(2 citation statements)

References 16 publications

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“…In the cerebral microcirculation of the cat, methylene blue specifically blocks endothelium-dependent dilation from acetylcholine without affecting the dilation from nitroglycerin, sodium nitroprusside, or nitric oxide.23 Selective blockade of endothelium-derived relaxing factor-mediated dilation also has been demonstrated in the femoral arteries of dogs in vivo24 and recently in vitro by investigators using cultured bovine aortic endothelial cells. 25 Our data are consistent with these recent observations made in animals. Methylene blue resulted in a reversal of the effect of acetylcholine on resistance vessels (from dilation to constriction).…”

Section: Discussionsupporting

confidence: 94%

Direct vasoconstriction and endothelium-dependent vasodilation. Mechanisms of acetylcholine effects on coronary flow and arterial diameter in patients with nonstenotic coronary arteries.

Hodgson¹,

Marshall²

1989

Circulation

190

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An endothelium-dependent vasodilator response to acetylcholine has been described recently in patients with coronary artery disease. Those studies determined responses only of large epicardial arteries. Our study was designed to determine the integrated effects of acetylcholine on epicardial diameter, coronary flow, and vascular resistance. Patients (n=64) with nonstenotic epicardial coronaries underwent coronary angiography with simultaneous recording of coronary flow velocity using a 3F subselective Doppler catheter. Measurements of epicardial arterial cross-sectional area (ECA), velocity, estimated flow (velocity times area), and vascular resistance were made before and after bolus administration of acetylcholine (100 ,ug i.c.). Similar measurements were made after papaverine (12-15 mg i.c.), a nonendothelium-dependent vasodilator. Acetylcholine resulted in a reduction of ECA of 19±3%, whereas papaverine increased ECA by 9±2%. Estimated flow increased 69±12% after acetylcholine and 147±12% after papaverine. Resistance fell after both agents (acetylcholine, -17+13%; papaverine, -61±2%). Transvascular resistance fell after acetylcholine in all but five patients. These patients had dramatic epicardial artery constriction (40±8% decrease in ECA). The effect of acetylcholine on both ECA and resistance was blocked by atropine (1 mg i.c.). Nitroglycerin (300 ,jg i.c.) resulted in epicardial dilatation (7.5±2.8%) in the same patients in whom acetylcholine caused constriction (-11.2+3.1%o). Pretreatment with methylene blue, an inhibitor of endothelium-derived relaxing factor (EDRF), potentiated epicardial artery vasoconstriction with acetylcholine (-25±7%o before versus -47±11% after, p

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Section: Discussionsupporting

confidence: 94%

Direct vasoconstriction and endothelium-dependent vasodilation. Mechanisms of acetylcholine effects on coronary flow and arterial diameter in patients with nonstenotic coronary arteries.

Hodgson¹,

Marshall²

1989

Circulation

190

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“…Indeed, Martin and Furchgott (Martin et al 14 ) suggested that this might be due, in part, to a direct action of methylene blue on EDRF. Also, Read and Dusting, 74 using cultured endothelial cells as a source of EDRF, found that methylene blue and hemoglobin blocked the EDRFmediated dilation from bradykinin but did not affect nitroglycerin-induced dilation. The simplest explanation for this differential action of methylene blue in in vivo experiments versus its effect in vitro is that smooth muscle permeability is high in some in vitro preparations and allows access by methylene blue to the cytosolic guanylate cyclase enzyme, whereas in vivo methylene blue is denied that access.…”

mentioning

confidence: 99%

Endothelium-derived relaxing factors. A perspective from in vivo data.

1990

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We review below published studies of endothelium-dependent vasodilation in vivo. Endothelium-dependent vasodilation has been demonstrated in conduit arteries in vivo and in the cerebral, coronary, mesenteric, and femoral vascular beds as well as in the microcirculation of the brain and the microcirculation of cremaster muscle. The available evidence, although not complete, strongly suggests that the endothellum-derived relaxing factor generated by acetylcholine in the cerebral microcirculation is a nitrosothiol. The endothelium-derived relaxing factor generated by bradykinin in this vascular bed is an oxygen radical generated in association with enhanced arachidonate metabolism via cyclooxygenase. In the microcirculation of skeletal muscle, on the other hand, the vasodilation from bradykinin is mediated partly by prostacycline and partly by an endothelium-derived relaxing factor similar to that generated by acetylcholine. Basal secretion of endothelium-derived relaxing factor is controversial in vivo but is usually present in vitro. On the other hand, it appears that endothelium-derived relaxing factor mediates flow-dependent vasodilation in both large vessels and in the microcirculation in vivo. The generation and release of endothelium-derived relaxing factor from endothelium may be abnormal in a variety of conditions including acute and chronic hypertension, atherosclerosis, and ischemia followed by reperfusion. Several mechanisms for these abnormalities have been identified. These include inability to generate endothelium-derived relaxing factor or destruction of endothelium-derived relaxing factor by oxidants after its release in the extracellular space. These abnormalities in endothelium-dependent relaxation may contribute to the vascular abnormalities in these conditions. (Hypertension 1990;16:371-386) T he discovery of endothelium-derived relaxing factor (EDRF) generated by acetylcholine 1 opened a new field of investigation into endothelium-derived vasoactive factors. It is now well established that a number of vasoactive agents indirectly induce vascular smooth muscle relaxation with ensuing vasodilation by acting on the endothelium to induce the generation and release of EDRFs. These substances are short-lived (Figure 1). Therefore, the final pathway for the vasodilation induced by EDRF is the same as that for the nitrodilators, which generate nitric oxide either spontaneously

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Cyclic nucleotide interactions involved in endothelium-dependent dilatation in rat aortic rings

Grace

Macdonald

Dusting

1988

European Journal of Pharmacology

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The Inhibitory Actions of Anti‐oxidants on Endothelium‐derived Relaxing Factor Released From Cultured Bovine Cells

Cited by 10 publications

References 16 publications

Direct vasoconstriction and endothelium-dependent vasodilation. Mechanisms of acetylcholine effects on coronary flow and arterial diameter in patients with nonstenotic coronary arteries.

Direct vasoconstriction and endothelium-dependent vasodilation. Mechanisms of acetylcholine effects on coronary flow and arterial diameter in patients with nonstenotic coronary arteries.

Endothelium-derived relaxing factors. A perspective from in vivo data.

Cyclic nucleotide interactions involved in endothelium-dependent dilatation in rat aortic rings

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