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β‐Adrenoceptor agonist mediated relaxation of rat isolated resistance arteries: a role for the endothelium and nitric oxide
Author(s) -
Graves J.,
Poston L.
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.tb12853.x
Subject(s) - agonist , nitric oxide , mesenteric arteries , endothelium , endocrinology , contraction (grammar) , chemistry , medicine , isoprenaline , nitric oxide synthase , stimulation , artery , receptor
1 Isoprenaline (10 −9 −10 −5 m ) relaxed rat isolated mesenteric resistance arteries pre‐contracted with K + (30–60 m m ) (p EC 50 ( m ) 8.03 ± 0.40; maximum relaxation 66.79 ± 2.43%, n = 7). This relaxation was partially attenuated by the nitric oxide (NO) synthase inibitor N ω ‐nitro‐ l ‐arginine methyl ester ( l ‐NAME, 10 −4 m ). 2 The β 2 ‐adrenoceptor agonist, salbutamol (10 −9 −10 −5 m ), produced a modest maximum relaxation (35.93 ± 2.93%), which was not sensitive to l ‐NAME. 3 The β 1 ‐adrenoceptor agonist, dobutamine (10 −9 −10 −5 m ), relaxed arteries precontracted with K + . This relaxation was abolished by l ‐NAME (10 −4 m ) and also by propranolol (10 −6 m ), but not affected by d ‐NAME (10 −4 m ). The inhibition by l ‐NAME was partially reversed by l ‐arginine (10 −3 m ). Removal of the endothelium severely attenuated relaxation to dobutamine. 4 Contractile responses to depolarizing K + solutions were enhanced by the addition of l ‐NAME, and also by removal of the endothelium. 5 The above findings demonstrate that β 1 ‐adrenoceptor activation causes relaxation via NO release from the endothelium of rat mesenteric resistance arteries. In addition, contraction to K + is modified by release of NO from the endothelium, possibly in response to tension development.