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(Circulation. 2004;110:2708-2712.)
© 2004 American Heart Association, Inc.

Vascular Medicine

Heterogeneous ß₂-Adrenoceptor Expression and Dilation in Coronary Arterioles Across the Left Ventricular Wall

Travis W. Hein, PhD^*; Cuihua Zhang, MD, PhD^*; Wei Wang, MD; Lih Kuo, PhD

From the Department of Medical Physiology, Cardiovascular Research Institute, College of Medicine, The Texas A&M University System Health Science Center, College Station, Tex.

Correspondence to Lih Kuo, PhD, Department of Medical Physiology, Cardiovascular Research Institute, College of Medicine, The Texas A&M University System Health Science Center, 702 Southwest H.K. Dodgen Loop, Temple, TX 76504. E-mail LKUO{at}tamu.edu

Received December 16, 2003; de novo received April 6, 2004; revision received May 24, 2004; accepted May 25, 2004.

Background— Previous in vivo studies have shown that ß-adrenoceptor agonists cause a redistribution of coronary flow away from the subendocardium; however, the underlying mechanism remains uncertain. We tested the hypothesis that a heterogeneous distribution of ß-adrenoceptors and their vasomotor responses exists in the coronary microcirculation across the left ventricular wall.

Methods and Results— Porcine subepicardial and subendocardial arterioles (<100 µm) were isolated from the left ventricle and pressurized for in vitro study of vasodilation to the nonselective ß-adrenoceptor agonist isoproterenol and the selective ß₂-adrenoceptor agonist procaterol. Both vessel types developed a similar level of basal tone and dilated to isoproterenol and procaterol. However, subepicardial arterioles exhibited a much higher sensitivity and greater dilation capacity to both agonists. The isoproterenol-induced vasodilations were inhibited by glibenclamide, an ATP-sensitive potassium (K_ATP) channel blocker. In contrast to isoproterenol, dilations of subepicardial and subendocardial arterioles to pinacidil, a K_ATP channel opener, were similar. In both vessel types, isoproterenol-induced dilation was inhibited by the ß₂-adrenoceptor blocker ICI-118,551 but was insensitive to the ß₁-adrenoceptor blocker atenolol. Reverse transcription–polymerase chain reaction and immunohistochemical data revealed that ß₂-adrenoceptor mRNA and protein expression, respectively, were markedly greater in subepicardial arterioles.

Conclusions— This study demonstrates that selective activation of ß₂-adrenoceptors elicits dilation of both subepicardial and subendocardial arterioles through opening of K_ATP channels. The higher ß₂-adrenoceptor expression in subepicardial arterioles may contribute to the greater dilation of these vessels to ß₂-adrenoceptor activation.

Key Words: receptors, adrenergic, beta • endocardium • microcirculation • vasodilation

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