期刊
JOURNAL OF GENERAL PHYSIOLOGY
卷 115, 期 5, 页码 653-662出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1085/jgp.115.5.653
关键词
calcium-induced calcium release; smooth muscle; Ca2+ sparks; excitation-contraction coupling; action potential signaling
类别
资金
- NHLBI NIH HHS [HL45239, R01 HL045239] Funding Source: Medline
- NIDDK NIH HHS [T32DK07708-06, T32 DK007708, DK52620, P50 DK052620] Funding Source: Medline
Calcium-induced calcium release (CICR) has been observed in cardiac myocytes as elementary calcium release events (calcium sparks) associated with the opening of L-type Ca2+ channels. In heart cells, a tight coupling between the gating of single L-type Ca2+ channels and ryanodine receptors (RYRs) underlies calcium release. Here we demonstrate that L-type Ca2+ channels activate RYRs to produce CICR in smooth muscle cells in the form of Ca2+ sparks and propagated Ca2+ waves. However, unlike CICR in cardiac muscle, RYR channel opening is not tightly linked to the gating of L-type Ca2+ channels. L-type Ca2+ channels can open without triggering Ca2+ sparks and triggered Ca2+ sparks are often observed after channel closure. CICR is a function of the net flux of Ca2+ ions into the cytosol, rather than the single channel amplitude of L-type Ca2+ channels. Moreover, unlike CICR in striated muscle, calcium release is completely eliminated by cytosolic calcium buffering. Thus, L-type Ca2+ channels are loosely coupled to RYR through an increase in global [Ca2+] due to an increase in the effective distance between L-type Ca2+ channels and RYR, resulting in an uncoupling of the obligate relationship that exists in striated muscle between the action potential and calcium release.
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