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Uniformity of calcium channel number and isometric contraction in human right and left ventricular myocardium

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Summary

We compared contractile performance in trabeculae carneae (n=25) from non-failing right and left ventricles (n=25) of brain dead organ donors without known cardiovascular disease and measured connective tissue content in trabeculae carneae from both non-failing and failing human hearts. Peak twitch force and time-course of contraction were not different between muscles taken from right or left ventricles. Peak twitch force was 13.9±3 vs. 13.7±2.7 mN/mm2 for right and left ventricular trabeculae carneae, respectively in 2.5 mM [Ca2+]0 at a 0.33 Hz stimulation frequency. Time to peak tension (405±21 vs. 405±12 ms), time to 50% relaxation from peak contractile response (277±21 vs. 278±14.6 ms) and time to 80% relaxation (428±29 vs. 433±22) were not different between right and left ventricular trabeculae carneae. Calcium channel number determined by [3H]PN200-100 dihydropyridine-radioligand binding assay was also not different (56.2±6.5 fmol/mg protein vs. 58.6±8.4 fmol/mg protein for right and left heart preparations, respectively). However, in myocardium obtained from ischemic hearts the left ventricle showed a reduced number of calcium channels compared to the right ventricle (55.3±3.8 vs. 36.6±3.9 fmol/mg protein for right and left ventricle, respectively p=0.027). No differences were noted in the number of DHP receptor binding sites between right and left ventricular myocardium from patients with idiopathic dilated cardiomyopathy (51.4±7.6 fmol/mg protein vs. 61.8±6.5 fmol/mg protein respectively). Our data indicate that calcium channel number is similar for non-failing left and right human ventricle. Contractile response to changes in [Ca2+]0 and frequency were similar for trabeculae carneae from the left and right ventricles of non-failing human hearts. Studies involving calcium channel activation or inhibition in ischemic human myocardium, where there may be differences in calcium channel number and/or function are warranted. Whether changes in calcium channel number have biological consequences on contractile function remains to be determined. Importantly, careful studies of calcium channel function underin vivo conditions are warranted.

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Author notes

  1. J. K. Gwathmey

    Present address: Cardiovascular Disease and Muscle Research Laboratories, Harvard Medical School, Building B1, Room 146, 220 Longwood Avenue, 02115, Boston, MA, USA

Authors and Affiliations

  1. Cardiovascular Disease and Muscle Research Laboratories, Harvard Medical School, Building B1, Room 146, 220 Longwood Avenue, 02115, Boston, MA, USA

    E. J. Grover

  2. Department of Medicine and Molecular and Cellular Physiology, Harvard Medical School, Building B1, Room 146, 220 Longwood Avenue, 02115, Boston, MA, USA

    J. K. Gwathmey

  3. Cardiovascular Division of the Beth Israel Hospital, Harvard Thorndike Laboratories of the Beth Israel Hospital, Boston, USA

    E. J. Grover, J. P. Morgan, B. S. Stambler & J. K. Gwathmey

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  1. E. J. Grover
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  2. J. P. Morgan
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  3. B. S. Stambler
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Additional information

Work supported in part by a grant from Glaxo Inc to JKG and the Institute for the Study of the Treatments of Cardiovascular Diseases, Cardiovascular Drug Development and Marketing Consultants, and HL-39091 and HL-36797 to JKG. HL 31117 to JPM. EJG is a fellow of the Stanley J. Sarnoff Society of Fellows for Research in Cardiovascular Science. JKG is an Established Investigator of the American Heart Association.

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Grover, E.J., Morgan, J.P., Stambler, B.S. et al. Uniformity of calcium channel number and isometric contraction in human right and left ventricular myocardium. Basic Res Cardiol 89, 139–148 (1994). https://doi.org/10.1007/BF00788733

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  • DOI: https://doi.org/10.1007/BF00788733

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