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Endogenous nitric oxide modulates adrenergic neural vasoconstriction in guinea‐pig pulmonary artery
Author(s) -
Liu S.F.,
Crawley D.E.,
Evans T.W.,
Barnes P.J.
Publication year - 1991
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.1476-5381.1991.tb12469.x
Subject(s) - prazosin , omega n methylarginine , phentolamine , vasoconstriction , endocrinology , medicine , contraction (grammar) , phenylephrine , nitric oxide , guanethidine , nitric oxide synthase , vasodilation , glibenclamide , chemistry , stimulation , antagonist , receptor , blood pressure , diabetes mellitus
1 Electrical field stimulation (EFS) of guinea‐pig isolated pulmonary artery induced a frequency‐dependent contraction. This was abolished by tetrodotoxin (1 μ m ) and prevented by phentolamine and prazosin (both 1 μ m ), indicating a role for α 1 ‐adrenoceptors activated by noradrenaline (NA) released from perivascular adrenergic nerves. 2 l ‐N G ‐monomethyl arginine ( l ‐NMMA, 0.3–100 μ m ) caused a concentration‐dependent enhancement of the EFS‐induced contraction with a 3.4 ± 0.5 fold increase at 100 μ m ( n = 6). The augmenting effect of 30 μ m l ‐NMMA on the contraction to EFS was completely reversed by 100–300 μ m l ‐arginine, but not by an identical concentration of d ‐arginine. 3 The contractile response to exogenous NA was similarly enhanced by 30 μ m l ‐NMMA (2.9 ± 0.6 fold increase, n = 5). 4 The contractile responses to exogenous phenylephrine and prostaglandin F 2α which matched the contraction to EFS (4 Hz) were equally augmented by 30 μ m l ‐NMMA. 5 In vessel rings submaximally contracted with the thromboxane analogue U44069 (2 μ m ), the selective α 2 ‐adrenoceptor agonist UK14304 induced concentration‐dependent relaxation, which was abolished by removal of endothelium. NA had little relaxant effect on these precontracted vessel rings unless in the presence of prazosin (1 μ m ). 6 Indomethacin had no significant effect on the contractile response to EFS or NA, indicating that vasodilator cyclo‐oxygenase products such as prostacyclin are not involved in modulating these responses. 7 Our results suggest that endogenous nitric oxide inhibits the contractile response to adrenergic nerve stimulation in the guinea‐pig pulmonary artery by a postjunctional mechanism, but release of prostacyclin does not modulate these responses. Basal release of nitric oxide from endothelial cells may account for this inhibition.