The mechanism of alpha-adrenergic activation of the dog coronary artery.
Norepinephrine (NE) activates isolated coronary conduit arteries by stimulating Ca2+ uptake into the smooth muscle cells. Blockade of Ca2+ influx by removal of Ca2+ from the bathing medium or addition of 10 mM LaCl3 prevents the NE-induced contraction in the dog coronary artery but still allows NE to induce a rapid transient contraction in the rabbit aorta. Under these conditions, NE stimulates 45Ca2+ efflux from rabbit aorta but fails to do so in the coronary artery. The difference in behaviour between the two arteries is attributed by the presence of an intracellular NE-sensitive Ca2+ fraction in the rabbit aorta and its absence from the dog coronary artery. This difference also explains the much greater sensitivity of the NE-induced contractions in the dog coronary to the relaxant effects of the Ca2+ antagonists, D600 and SKF525A, than that seen in the rabbit aorta. High K+-induced contractions of both the coronary artery and the aorta are equally sensitive to the Ca2+ antagonists.
D000818:Animals; D001011:Aorta / Q000187:drug effects; D002118:Calcium / Q000494:pharmacology; D003331:Coronary Vessels / Q000187:drug effects*; D004285:Dogs; D004533:Egtazic Acid / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D011335:Proadifen / Q000494:pharmacology; D011817:Rabbits; D011941:Receptors, Adrenergic; D011942:Receptors, Adrenergic, alpha
D011941:Receptors, Adrenergic; D011942:Receptors, Adrenergic, alpha; D004533:Egtazic Acid; D011335:Proadifen; D002118:Calcium; D009638:Norepinephrine