Predominant α₁adrenoceptor-mediated contraction in the human internal mammary artery

α-Adrenoceptor agonists and antagonists are widely used perioperatively for internal mammary artery (IMA)-coronary artery bypass operations. To determine subtypes of a-adrenoceptors in the human IMA, we studied responses of isolated human IMA segments to a-adre-noceptor agonists, antagonists, and electrical stimulation in organ baths. The IMA ring segments (3 mm long) were set up at a physiologic and comparable condition according to their own length-tension curves. α₁Agonist meth-oxamine (MO) induced 2.65 ± 0.70 g force and α₁α₂-agonist norepinephrine (NE) induced 4.07 ± 0.70 g force. The contractions induced by both MO and NE were totally abolished by ai-antagonist prazosin (0.1 µM) but not α₂-antagonist yohimbine. α₂-Agonist UK14304 induced only 0.39 ± 0.17 g force, which was significantly less than that induced by MO or NE (p < 0.001). Contractions induced by electrical field stimulation (2, 10, 20 Hz) were decreased by α₁-antagonist prazosin 1 µM (p < 0.01) but potentiated by α₂-antagonist yohimbine. These results strongly suggest that in the human IMA the postjunctional α-adrenoceptors are predominantly of the α₁-subtype and therefore the α-adrenoceptor agonist-induced contraction and the sympathetic nerve stimulation-induced contraction is mediated mainly by activation of the α₁-adrenoceptors.