Studies on the mechanisms underlying β-adrenoceptor-mediated relaxation of rat abdominal aorta

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Mechanisms underlying β-adrenoceptor (β-AR)-mediated vascular relaxation were studied in the isolated rat abdominal aorta. In the endothelium-denuded helical preparations, a non-selective β-AR agonist isoprenaline elicited a concentration-dependent relaxation. In the absence of β-AR antagonists, isoprenaline-induced relaxation was not practically affected by an adenylyl cyclase inhibitor SQ 22,536 (300 μM), but was strongly diminished by high-KCl (80 mM). Isoprenaline-induced relaxation in the presence of SQ 22,536 was significantly diminished by iberiotoxin (IbTx, 0.1 μM), but was not affected by 4-aminopyridine (4-AP, 3 mM). Isoprenaline-induced relaxation was not also affected by SQ 22,536 (300 μM) even in the presence of CGP20712A (a β_1-selective antagonist) and ICI-118,551 (a β_2-selective antagonist) (0.1 μM for each), but was strongly diminished by high-KCl. By contrast, SQ 22,536-resistant, isoprenaline-induced relaxation in the presence of CGP20712A plus ICI-118,551 was not affected by IbTx (0.1 μM), but was inhibited significantly by 4-AP (3 mM). These results suggest that in rat abdominal aortic smooth muscle: 1) both β_1-/β_2-AR- and β_3-AR-mediated relaxations substantially involve cAMP-independent mechanisms; 2) β_1-/β_2-AR-mediated, cAMP-independent relaxant mechanisms are partly attributed to the large-conductance, Ca^<2+>-sensitive K^+ (MaxiK, BK) channel whereas β_3-AR-mediated relaxant mechanisms are attributed to K_v channel.
日本平滑筋学会の論文

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