Endothelin-1- and endothelin-3-induced vasorelaxation via endothelium-derived nitric oxide

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The Possible Involvement of Nitric Oxide/Endothelium Derived Relaxing Factor in Atropine-Induced Vasorelaxation

Atropine has been used to block cholinergic neurotransmission in basic research. Large doses of atropine cause vasodilation of the blood vessels in the skin. This effect is apparently unconnected with the antimuscarinic activity of atropine and seems to be due to a direct action on the blood vessels. It has been suggested that atropine blocks muscarinic receptors at low doses and it induces th...

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Endothelium-Derived Nitric Oxide and Enhanced Vasoconstriction to Exogenously Administered Endothelin-1 in Clinically Healthy Smokers

Background Smoking is a major risk factor for the development of atherosclerosis. Because endothelial dysfunction may be a marker for future atherosclerosis, we investigated the effects of smoking on endothelium-dependent control of vascular tone. Methods and Results The effects of brachial arterial infusions of N0-monomethyl-L-arginine (L-NMMA), a nitric oxide synthesis inhibitor; sodium nitro...

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the possible involvement of nitric oxide/endothelium derived relaxing factor in atropine-induced vasorelaxation

atropine has been used to block cholinergic neurotransmission in basic research. large doses of atropine cause vasodilation of the blood vessels in the skin. this effect is apparently unconnected with the antimuscarinic activity of atropine and seems to be due to a direct action on the blood vessels. it has been suggested that atropine blocks muscarinic receptors at low doses and it induces the...

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Nitric oxide-endothelin-1 interaction in humans.

Healthy men received NG-monomethyl-L-arginine (L-NMMA) intravenously to study cardiovascular and metabolic effects of nitric oxide synthase blockade and whether this alters the response to endothelin-1 (ET-1) infusion. Controls only received ET-1. L-NMMA effects were that heart rate (17%) cardiac output (17%), and splanchnic and renal blood flow (both 33%) fell promptly (all P < 0.01). Mean art...

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Endothelium-derived endothelin-1 reduces cerebral artery sensitivity to nitric oxide by a protein kinase C-independent pathway.

BACKGROUND AND PURPOSE Nitric oxide (NO) reduces endothelin-1 (ET-1) production and blunts ET-1 dependent vasoconstriction. The direct effects of smooth muscle ET(A) receptor stimulation on NO-mediated relaxation are unknown. We hypothesized that endothelium-derived ET-1 regulates vascular tone by reducing smooth muscle sensitivity to NO, possibly through activation of protein kinase C (PKC). ...

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ژورنال

عنوان ژورنال: Japanese Journal of Pharmacology

سال: 1992

ISSN: 0021-5198

DOI: 10.1016/s0021-5198(19)59987-5