Endothelium-Removal Decreases Relaxations of Canine Coronary Arteries Caused by β-Adrenergic Agonists and Adenosine

Abstract

Experiments were designed to investigate the importance of the endothelium in relaxation of isolated coronary arteries caused by .beta.-adrenoceptor agonists or adenosine. Rings of canine left circumflex coronary arteries were suspended for isometric tension recording in organ chambers filled with physiological salt solution. Norepinephrine, isoproterenol, adenosine, acetylcholine and sodium nitroprusside caused relaxations of control rings contracted with prostaglandin F2.alpha. or KCl. The relaxations to all substances tested were relatively smaller during contractions evoked by KCl than those caused by prostaglandin F2.alpha.. Mechanical removal of the endothelium abolished the relaxations caused by acetylcholine, reduced those caused by the catecholamines and adenosine and did not affect the relaxations to sodium nitroprusside during contractions to prostaglandin F2.alpha.. Endothelium-removal did not affect relaxations to .beta.-adrenergic agonists or adenosine during contractions to KCl or after pretreatment of the arteries with indomethacin. Indomethacin did not affect responses to acetylcholine or sodium nitroprusside, but augmented those in response to .beta.-adrenoceptor stimulation and adenosine. The endothelial cells of the canine coronary artery evidently produce a signal in response to .beta.-adrenergic agonists and adenosine, which facilitates the direct inhibitory action of these substances on vascular smooth muscle.