Ca(2+)-signaling in cardiac myocytes: evidence from evolutionary and transgenic models.
Cardiac contraction is regulated by a number of Ca(2+)-mediated processes. Here we consider the effects of modification imposed on the Ca(2+)-signalling mechanism by evolutionary developments and transgenic manipulations. Ca(2+)-signalling appears to be mediated via influx of Ca2+ through the DHP receptor in preference to the Na(+)-Ca2+ exchange protein, and activates the ryanodine receptor and the Ca2+ release from the SR. Here we report on functional consequences of overexpression of the Na(+)-Ca2+ exchanger and calsequestrin. The data does not support a physiological role for the Na(+)-Ca2+ exchanger in signalling Ca2+ release, but can serve to modify ionic currents which determine the duration of the action potential.
Morad
M
M
Department of Pharmacology, Georgetown University Medical Center, Washington, DC 20007-2197, USA.
Suzuki
Y J
YJ
D000818:Animals; D030801:Animals, Genetically Modified; D005075:Biological Evolution; D002118:Calcium / Q000378:metabolism*; D002155:Calsequestrin / Q000235:genetics / Q000502:physiology; D015870:Gene Expression; D006321:Heart / Q000502:physiology*; D006801:Humans; D008954:Models, Biological; D009206:Myocardium / Q000166:cytology*; D015398:Signal Transduction; D019831:Sodium-Calcium Exchanger / Q000235:genetics / Q000502:physiology
D002155:Calsequestrin; D019831:Sodium-Calcium Exchanger; D002118:Calcium