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—
Methods and Results—Administration of the
Conclusions—Cardiac myocytes have a requisite role in
constriction of coronary resistance vessels to
© 1998 American Heart Association, Inc.
Brief Rapid Communications
Requisite Role of Cardiac Myocytes in Coronary
1-Adrenergic Constriction
-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). 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. 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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