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Updated: Aug 9, 2026

Isolation of Atrial Myocytes from Adult Mice
Published on: July 25, 2019
Requisite role of cardiac myocytes in coronary alpha1-adrenergic constriction
C P Tiefenbacher1, D V DeFily, W M Chilian
1Department of Physiology, Medical College of Wisconsin, Milwaukee 53226, USA.
Insights
Cardiac myocytes play a key role in alpha1-adrenergic coronary arteriolar constriction. Myocyte-released factors, potentially including endothelin-1, mediate this response, unlike direct stimulation of microvessels.
Area of Science:
- Cardiovascular Physiology
- Vascular Biology
- Adrenergic Signaling
Background:
- Alpha-adrenergic activation typically constricts coronary arterioles in vivo.
- Isolated coronary microvessels paradoxically do not contract to alpha1-adrenergic stimuli in vitro.
Purpose of the Study:
- To investigate the role of cardiac myocytes in alpha1-adrenergic coronary arteriolar constriction.
- To identify potential myocyte-derived factors mediating this vasoconstriction.
Main Methods:
- Isolated coronary arterioles were exposed to phenylephrine or supernatant from phenylephrine-treated cardiac myocytes.
- Antagonists for endothelin-A and alpha-adrenergic receptors were used.
- Adenosine antagonist was administered.
- Endothelin-1 levels in myocyte supernatant were measured.
Main Results:
- Phenylephrine did not constrict isolated arterioles directly.
- Supernatant from treated myocytes induced arteriolar constriction.
- Constriction was blocked by endothelin-A and alpha-adrenergic antagonists.
- Adenosine antagonism augmented constriction.
- Phenylephrine increased myocyte endothelin-1 to subthreshold levels.
Conclusions:
- Cardiac myocytes are essential for alpha1-adrenergic coronary resistance vessel constriction.
- The mechanism may involve endothelin-1 and other unidentified myocyte-derived vasoconstrictors.
Background:
Alpha-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 alpha1-adrenergic coronary arteriolar constriction through the release of myocyte-derived contractile factor(s).
Methods And Results:
Administration of the alpha1-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 alpha-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 alpha1-adrenergic stimuli, which may be mediated by endothelin-1 and other unidentified myocyte-derived vasoconstrictors.
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