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Alpha-2 adrenergic receptors stimulate actin organization in developing fetal rat cardiac myocytes

Posted by on in 2003
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Life Sciences, Volume 72, Issue 13 , 14 February 2003, Pages 1455-1466
Amy C. Porter (a), Samuel P. S. Svensson (a)(1), W. Daniel Stamer (a)(2), Joseph J. Bahl (b), Jeremy G. Richman (a)(3) and John W. Regan (a)
(a) Departments of Pharmacology & Toxicology, Physiology and the Program in Neuroscience, College of Pharmacy, The University of Arizona, Tucson, AZ 85721, USA
(b) Internal Medicine, University Heart Center, College of Medicine, The University of Arizona, Tucson, AZ 85721, USA
Received 4 December 2001; accepted 6 September 2002; Available online 7 January 2003.
(1) Present address: AstraZeneca R&D, Sodertalje, Sweden.
(2) Present address: The University of Arizona, Department of Ophthalmology, 655 N. Alvernon Way, Suite 108, Tucson, AZ 85711.
(3) Present address: Arena Pharmaceuticals, Inc., 6166 Nancy Ridge Dr., San Diego, CA 92121.

Abstract

Expression of 2-adrenergic receptors (2-AR) is very high in fetal rat heart although numbers decline with increasing gestational age. The current experiments were designed to identify the subtypes of 2-AR expressed and the function of these receptors in fetal cardiac myocytes. Expression of 2A and 2C, but not 2B, was confirmed in the myocyte population by indirect immunofluorescence microscopy with subtype-specific antibodies and by Western blot. Both dexmedetomidine, an 2-selective agonist, and norepinephrine, increased actin cytoskeleton organization and this increase was blocked by the 2-selective antagonist, atipamezole. Furthermore, dexmedetomidine inhibited isoproterenol-stimulated cAMP accumulation in isolated fetal rat heart and this was blocked by rauwolscine. Therefore, functional 2A and 2B subtypes are present in the fetal rat heart where they may have a role in cardiac development.

Author Keywords: Fetal heart; 2-adrenergic receptors; Cytoskeleton; Actin; Phalloidin; Immunocytochemistry

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