Increased release of nitric oxide in ischemic hearts after exercise in patients with effort angina (Q74787732)

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13 November 2019

title

Increased release of nitric oxide in ischemic hearts after exercise in patients with effort angina (English)

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13 November 2019

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K Node

1

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M Kitakaze

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13 November 2019

H Sato

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Y Koretsune

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M Karita

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H Kosaka

6

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M Hori

7

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13 November 2019

language of work or name

English

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publication date

1 July 1998

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Journal of the American College of Cardiology

13 November 2019

published in

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13 November 2019

volume

32

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13 November 2019

issue

1

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13 November 2019

page(s)

63-68

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Inhibition of nitric oxide production aggravates myocardial hypoperfusion during exercise in the presence of a coronary artery stenosis.

13 November 2019

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Ischemia, hyperemia, exercise, and nitric oxide. Complex physiology and complex molecular adaptations

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Nitric oxide release accounts for the biological activity of endothelium-derived relaxing factor

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Hypoxic coronary vasodilatation and cGMP overproduction are blocked by a nitric oxide synthase inhibitor, but not by a guanylyl cyclase ANF receptor antagonist

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Nitric oxide is a mediator of hypoxic coronary vasodilatation. Relation to adenosine and cyclooxygenase-derived metabolites

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Inhibition of hypoxia-induced relaxation of rabbit isolated coronary arteries by NG-monomethyl-L-arginine but not glibenclamide

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Role of EDRF in the regulation of regional blood flow and vascular resistance at rest and during exercise in conscious dogs

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Acute effects of nitrates on exercise testing in patients with syndrome X. Clinical and pathophysiological implications

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Direct measurement of nitric oxide generation in the ischemic heart using electron paramagnetic resonance spectroscopy

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Increased release of NO during ischemia reduces myocardial contractility and improves metabolic dysfunction

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Plasma nitric oxide end products are increased in the ischemic canine heart.

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Paradoxical vasoconstriction induced by acetylcholine in atherosclerotic coronary arteries

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Evidence of impaired endothelium-dependent coronary vasodilatation in patients with angina pectoris and normal coronary angiograms.

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The rate-pressure product as an index of myocardial oxygen consumption during exercise in patients with angina pectoris

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Shear stress elevates endothelial cGMP. Role of a potassium channel and G protein coupling

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Nitric oxide is responsible for flow-dependent dilatation of human peripheral conduit arteries in vivo

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Identifiers

DOI

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13 November 2019

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