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(Circulation. 1998;98:9-12.)
© 1998 American Heart Association, Inc.

Brief Rapid Communications

Requisite Role of Cardiac Myocytes in Coronary ₁-Adrenergic Constriction

Christiane P. Tiefenbacher, MD; David V. DeFily, PhD; ; William M. Chilian, PhD

From the Department of Physiology, Medical College of Wisconsin, Milwaukee. Dr Tiefenbacher is now at the Medizinische Klinik III/Kardiologie, Universität Heidelberg, Germany. Dr DeFily is now at the Center for Anesthesiology Research, Cleveland Clinic Foundation, Cleveland, Ohio.

Correspondence to William M. Chilian, PhD, Department of Physiology, Medical College of Wisconsin, 8701 Watertown Plank Rd, Milwaukee, WI 53226. E-mail chilian{at}post.its.mcw.edu

Background—-Adrenergic activation in vivo causes constriction of coronary arterioles, but, paradoxically, in vitro these microvessels do not contract to this stimulus. We hypothesized that cardiac myocytes have a requisite role in ₁-adrenergic coronary arteriolar constriction through the release of myocyte-derived contractile factor(s).

Methods and Results—Administration of the ₁-adrenergic agonist phenylephrine did not constrict isolated coronary arterioles, but constriction was observed to supernatant obtained from phenylephrine-treated cardiac myocytes. Constriction to the supernatant was blocked by administration of an endothelin-A antagonist to the microvessel preparation or an -adrenergic antagonist to the myocytes and was augmented after administration of an adenosine antagonist. Administration of phenylephrine to the myocytes increased endothelin-1 levels in the supernatant, but only to subthreshold concentrations.

Conclusions—Cardiac myocytes have a requisite role in constriction of coronary resistance vessels to ₁-adrenergic stimuli, which may be mediated by endothelin-1 and other unidentified myocyte-derived vasoconstrictors.

Key Words: microcirculation • endothelin • phenylephrine • dogs

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