Weak beta-adrenoceptor-mediated relaxation in the human internal mammary artery.

The function of beta-adrenoceptors in the human internal mammary artery was studied in vitro to predict the way in which the internal mammary artery graft would respond to beta-adrenergic agonists and antagonists given in the perioperative period. Ring segments of the distal internal mammary artery obtained from patients not receiving beta-blocker therapy were mounted in organ baths and isometric wall force was measured. For comparison, similar experiments were conducted on segments of canine coronary artery, a vessel known to have powerful beta-adrenoceptor function. All arteries were precontracted with potassium or the thromboxane mimetic agent, U46619, before isoproterenol cumulative concentration-relaxation curves were constructed. In the human internal mammary artery, the maximum relaxation induced by isoproterenol was only 14% of the potassium-induced contraction and 24% of the U46619-induced contraction. These responses were weak compared with 54% and 86% for beta-adrenoceptor relaxation measured in corresponding experiments in the canine coronary artery. In all experiments, propranolol antagonized the relaxation induced by isoproterenol. These studies suggested that the human internal mammary artery has only a small number of beta-adrenoceptors. We conclude that beta-adrenoceptors would contribute little to the reactivity of the human internal mammary artery graft to sympathomimetic drugs.