| First Author | Yao A | Year | 1998 |
| Journal | J Mol Cell Cardiol | Volume | 30 |
| Issue | 12 | Pages | 2711-8 |
| PubMed ID | 9990541 | Mgi Jnum | J:127827 |
| Mgi Id | MGI:3765118 | Doi | 10.1006/jmcc.1998.0834 |
| Citation | Yao A, et al. (1998) Sarcoplasmic reticulum function in murine ventricular myocytes overexpressing SR CaATPase. J Mol Cell Cardiol 30(12):2711-8 |
| abstractText | To examine the effects of the overexpression of sarcoplasmic reticulum (SR) CaATPase on function of the SR and Ca2+ homeostasis, we measured [Ca2+]i transients (fluo-3), and L-type Ca2+ currents (ICa.L), Na/Ca exchanger currents (INa/Ca), and SR Ca2+ content with voltage clamp in ventricular myocytes isolated from wild type (WT) mice and transgenic (SRTG) mice. The amplitude of [Ca2+]i transients was insignificantly increased in SRTG myocytes, while the diastolic [Ca2+]i tended to be lower. The initial and terminal declines of [Ca2+]i transients were significantly accelerated in SRTG myocytes, implying a functional upregulation of the SR CaATPase. We examined the functional contribution of only the SR CaATPase to the initial and the terminal phase of the decline of [Ca2+]i, by abruptly inhibiting Na/Ca exchange with a rapid switcher device. The rate of [Ca2+] decline mediated by the SR CaATPase was increased by 40% in SRTG compared with WT myocytes. The function of the L-type Ca2+ channel was unchanged in SRTG myocytes, while INa/Ca density was slightly (10%) decreased. Measured SR Ca2+ content was significantly increased by 29% in SRTG myocytes. Thus, overexpression of SR CaATPase markedly accelerates the decline of [Ca2+]i transients, and induces in increase in SR Ca2+ content, with some downregulation of the Na/Ca exchanger. |
