Uniformity of calcium channel number and isometric contraction in human right and left ventricular myocardium.
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 under in vivo conditions are warranted.
Gruver
E J
EJ
Cardiovascular Disease and Muscle Research Laboratories, Harvard Medical School.
Morgan
J P
JP
Stambler
B S
BS
Gwathmey
J K
JK
D000293:Adolescent; D000328:Adult; D015220:Calcium Channels / Q000032:analysis / Q000502:physiology*; D009202:Cardiomyopathies / Q000503:physiopathology*; D002311:Cardiomyopathy, Dilated / Q000503:physiopathology; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D008875:Middle Aged; D009200:Myocardial Contraction; D016277:Ventricular Function, Left / Q000502:physiology; D016278:Ventricular Function, Right / Q000502:physiology
D015220:Calcium Channels