Responses of Coronary Smooth Muscle to Catecholamines

Abstract

Responses to catecholamines were studied in isolated helical muscle strips of large and small coronary vessels and in isolated perfused coronary arteries from the dog. Epinephrine and norepinephrine in concentrations well below those normally present in the blood uniformly caused relaxation of small coronary vessels. Norepinephrine was much more potent than epinephrine. The relaxation was reversibly blocked by the beta adrenergic blocker, nethalide. During this blockade, catecholamines either were inactive or produced a slight contraction. Strips contracted by angiotensin, blood or KCl, as well as those completely depolarized by K 2 SO 4 , were relaxed by catecholamines. Strips taken from large coronary vessels, unlike those from small vessels, were, in some cases, contracted by catecholamines; in others, after a transient contraction, they were relaxed. Contraction was blocked by Dibenzyline. This difference in behavior of large and small vessels may account for some of the contradictions found in the literature concerning the response of coronary vessels to catecholamines.

Characterization of the coronary vascular β‐adrenoceptor in the pig

“…These difficulties can be avoided by removing the coronary vessels from the myocardium and observing the direct effects of adrenoceptor agonists and antagonists on the vascular smooth muscle in vitro (Zuberbuhler & Bohr, 1965;Bohr, 1967). In the present work, the /3-adrenoceptor in pig isolated coronary artery strips has been characterized by the use of salbutamol, an agonist with selectivity for peripheral vascular /8-adrenoceptors (/32 type) and practolol, an antagonist with selectivity for myocardial /3-adrenoceptors (#,-type).…”

“…KCl producing 0-6-0-8 g increase in tension. In a previous study it was shown that the relaxant effect of catecholamines on coronary artery strips is unaffected by the type of spasmogen used (Zuberbuhler & Bohr, 1965 Antagonist potencies of propranolol and practolol were determined with isoprenaline as the agonist. Two or three control cumulative concentration-effect curves for isoprenaline were obtained and the antagonist added to the bathing solution for 45 min before responses to isoprenaline were re-examined.…”

Responses of isolated dog coronary arteries to tyramine.

“…Coronary arteries used were of intermediate sizes in comparison with small (0.25 to 0.5 mm) and large (1.5 to 2.4 mm) arteries reported by Zuberbuhler and Bohr (6). These arteries were expected to show both contractile and relaxant responses to endogenous norepin ephrine.…”

“…It seems likely that the tyramine (2x10-5 M or higher) -induced contraction is not mediated by norepin ephrine released, but it is partly due to a direct action on alpha-adrenoceptors. (5,6). Exogenous norepinephrine preferentially stimulates excitatory alpha -adrenoceptors in large coronary arteries but inhibitory beta adrenoceptors in small arteries (6)(7)(8)(9).…”

“…(5,6). Exogenous norepinephrine preferentially stimulates excitatory alpha -adrenoceptors in large coronary arteries but inhibitory beta adrenoceptors in small arteries (6)(7)(8)(9). Dog coronary arteries are adrenergically innervated (10,11).…”