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Influences of the endothelium and hypoxia on neurogenic transmission in the isolated pulmonary artery of the rabbit
Author(s) -
MacLean Margaret R.,
McCulloch K.M.,
MacMillan J.B.,
McGrath J.C.
Publication year - 1993
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1993.tb13455.x
Subject(s) - rauwolscine , prazosin , nitric oxide , nitric oxide synthase , endothelium , hypoxia (environmental) , endocrinology , contraction (grammar) , medicine , nitroarginine , omega n methylarginine , chemistry , antagonist , pharmacology , biology , receptor , oxygen , organic chemistry
1 The effects of nitric oxide (10 −6 m ), N ω ‐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 (α 1 ‐adrenoceptor antagonist) and unaffected by rauwolscine (α 2 ‐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 α 2 ‐adrenoceptors in EFS‐induced contraction. Hypoxia inhibited neurogenic responses in rabbit isolated pulmonary arteries.