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PMID: 1648625 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Dihydropyridine receptor binding sites in the cardiomyopathic hamster heart are unchanged from control.

Journal of molecular and cellular cardiology ·Vol. 23 ·No. 2 ·1991-02-00 ·Pages 111-7

Bazan E, Sole MJ, Schwartz A, Johnson CL

Abstract

An increase in the number of voltage dependent calcium channels has been implicated in the overload of calcium found in cardiac tissue of the cardiomyopathic hamster. We examined the binding of [3H]-(+)PN200110 to dihydropyridine receptors in cardiac muscle membranes from TO cardiomyopathic hamsters. When compared to random bred controls, there were no differences in either the Bmax or the KD for [3H]-(+)PN200110 binding using homogenates from 35 to 41-day-old TO cardiomyopathic hearts. In 8 to 9-month-old myopathic animals there were only small decreases in Bmax with no change in KD. We suggest that the calcium overload observed in cardiomyopathic hamster heart may not be due to an increased density of calcium channels as estimated by high affinity dihydropyridine receptor binding sites.

MeSH Terms
Animals Calcium Channel Blockers/metabolism Calcium Channels/metabolism Cardiomyopathies/metabolism Cricetinae Isradipine Male Myocardium/metabolism Oxadiazoles/metabolism Receptors, Nicotinic/metabolism
Chemicals
Calcium Channel Blockers Calcium Channels Oxadiazoles Receptors, Nicotinic Isradipine
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Bazan E
Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, OH 45267-0575.
Sole M J
Schwartz A
Johnson C L
Article Info
Journal
Journal of molecular and cellular cardiology
Abbr.
J Mol Cell Cardiol
ISSN
0022-2828
Published
1991-02-00
Pages
111-7
Language
English
Region
England
NLM ID
0262322
Subset
IM
Grants
NHLBI NIH HHS · P01 HL22619-11 · United States
Corrections
CommentIn
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