title: Heterogeneous beta2-adrenoceptor expression and dilation in coronary arterioles across the left ventricular wall.
abstract: BACKGROUND
  Previous in vivo studies have shown that beta-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 beta-adrenoceptors and their vasomotor responses exists in the coronary microcirculation across the left ventricular wall.
  
  
  RESULTS
  Porcine subepicardial and subendocardial arterioles (<100 microm) were isolated from the left ventricle and pressurized for in vitro study of vasodilation to the nonselective beta-adrenoceptor agonist isoproterenol and the selective beta2-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 beta2-adrenoceptor blocker ICI-118,551 but was insensitive to the beta1-adrenoceptor blocker atenolol. Reverse transcription-polymerase chain reaction and immunohistochemical data revealed that beta2-adrenoceptor mRNA and protein expression, respectively, were markedly greater in subepicardial arterioles.
  
  
  CONCLUSIONS
  This study demonstrates that selective activation of beta2-adrenoceptors elicits dilation of both subepicardial and subendocardial arterioles through opening of K(ATP) channels. The higher beta2-adrenoceptor expression in subepicardial arterioles may contribute to the greater dilation of these vessels to beta2-adrenoceptor activation.
authors.affiliation: 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. LKUO@tamu.edu.
authors.forename: Travis W
authors.initials: TW
authors.lastname: Hein
authors.forename: Cuihua
authors.initials: C
authors.lastname: Zhang
authors.forename: Wei
authors.initials: W
authors.lastname: Wang
authors.forename: Lih
authors.initials: L
authors.lastname: Kuo
mesh_terms: D058666:Adrenergic beta-2 Receptor Agonists; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D001160:Arterioles / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D003331:Coronary Vessels / Q000378:metabolism / Q000502:physiology*; D005905:Glyburide / Q000494:pharmacology; D006352:Heart Ventricles / Q000378:metabolism*; D026902:Potassium Channel Blockers / Q000494:pharmacology; D017265:Procaterol / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D018343:Receptors, Adrenergic, beta-2 / Q000235:genetics / Q000378:metabolism*; D013552:Swine; D014664:Vasodilation / Q000187:drug effects
chemical_list: D058666:Adrenergic beta-2 Receptor Agonists; D000318:Adrenergic beta-Agonists; D026902:Potassium Channel Blockers; D012333:RNA, Messenger; D018343:Receptors, Adrenergic, beta-2; D005905:Glyburide; D017265:Procaterol