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In coronary arterial rings isolated from horse, norepinephrine (NE)(10(-7) - 10(-5) M) induced concentration-dependent contractions which were not influenced by endothelial denudation. Prazosin (alpha 1-antagonist) inhibited the contraction, but yohimbine (alpha 2-antagonist) did not, and propranolol (beta-antagonist) enhanced the contraction. Pretreatment with phentolamine (10(-5) M) (alpha-antagonist) converted the contraction induced by NE to relaxation in coronary rings precontracted with ONO11113 (thromboxane A2 derivative). The relaxation was not influenced by removal of the endothelium, and was inhibited by propranolol and atenolol (beta 1-antagonist) but not by butoxamine (beta 2-antagonist). These results suggest that in equine coronary arteries, the contractile response to NE is mediated by stimulation of alpha 1-adrenoceptors on the smooth muscle, and that stimulation of beta 1-adrenoceptors on the smooth muscle modifies the contraction by inducing relaxation.

Participation of .ALPHA.1- and .BETA.1-Adrenoceptors in Norepinephrine-Induced Contraction and Relaxation of Isolated Equine Coronary Artery in Vitro.