Role of non-nitric oxide non-prostaglandin endothelium-derived relaxing factor(s) in bradykinin vasodilation

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Role of non-nitric oxide non-prostaglandin endothelium-derived relaxing factor(s) in bradykinin vasodilation.

The most conspicuous effect of bradykinin following its administration into the systemic circulation is a transient hypotension due to vasodilation. In the present study most of the available evidence regarding the mechanisms involved in bradykinin-induced arterial vasodilation is reviewed. It has become firmly established that in most species vasodilation in response to bradykinin is mediated ...

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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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The identification of nitric oxide as endothelium-derived relaxing factor.

The identification of endothelium-derived relaxing factor as nitric oxide (NO) dramatically altered the course of vascular biology, as well as other biomedical disciplines. The ubiquity of this natural product of cell metabolism and the complexity of its biochemistry provide a rich source of molecular mediators of phenotype in health and disease.

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Contribution of endothelium-derived nitric oxide to exercise-induced vasodilation.

BACKGROUND Endothelium-derived nitric oxide is an important modulator of resting vascular tone in animals and humans. However, the contribution of nitric oxide to exercise-induced vasodilation is unknown. METHODS AND RESULTS The effect of NG-monomethyl-L-arginine (L-NMMA), an inhibitor of nitric oxide synthesis, on exercise-induced vasodilation was studied in 18 healthy subjects (mean +/- SD,...

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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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ژورنال

عنوان ژورنال: Brazilian Journal of Medical and Biological Research

سال: 1998

ISSN: 0100-879X

DOI: 10.1590/s0100-879x1998000900017