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• W2021145278 abstract "1 The effects of nitric oxide (10−6 m), Nω-nitro-l-arginine methylester (l-NAME, 10−4 m, an inhibitor of nitric oxide synthase), endothelium removal, hypoxia and selective α-adrenoceptor antagonists on responses to nerve electrical field-stimulation (EFS) were studied in the rabbit isolated pulmonary artery. 2 EFS induced frequency-dependent contractions which were abolished by prazosin (α1-adrenoceptor antagonist) and unaffected by rauwolscine (α2-adrenoceptor antagonist). EFS-induced responses were potentiated by l-NAME and inhibited by nitric oxide. The effect of l-NAME was reversed by the presence of l-arginine (2 × 10−4 m), which had no effect on its own. In the presence of l-NAME, the EFS-induced responses were reduced by rauwolscine and the residual responses were abolished by prazosin. 3 Removal of the vascular endothelium increased the maximum contractile response to EFS but did not inhibit the ability of l-NAME to potentiate contractile responses to EFS. 4 Hypoxia inhibited the contractile response to EFS. This effect of hypoxia was also seen in the presence of l-NAME and in endothelium rubbed preparations. 5 In conclusion, the endothelium modulates EFS-induced contractions in the rabbit pulmonary artery. The contraction induced by EFS was inhibited by nitric oxide, but potentiated by the nitric oxide-synthase inhibitor, l-NAME. The effect of l-NAME was not mediated solely through the endothelium and revealed involvement of α2-adrenoceptors in EFS-induced contraction. Hypoxia inhibited neurogenic responses in rabbit isolated pulmonary arteries." @default.
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• W2021145278 date "1993-01-01" @default.
• W2021145278 modified "2023-09-25" @default.
• W2021145278 title "Influences of the endothelium and hypoxia on neurogenic transmission in the isolated pulmonary artery of the rabbit" @default.
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• W2021145278 doi "https://doi.org/10.1111/j.1476-5381.1993.tb13455.x" @default.
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