Abstract
This review discusses the control of the amplitude of the cardiac systolic Ca transient. The Ca transient arises largely from release from the sarcoplasmic reticulum (SR). Release is triggered by calcium-induced calcium release (CICR) whereby the entry of a small amount of Ca on the L-type Ca current, "the trigger", results in the release of much more Ca from the SR. There are three potential control points: (1) the Ca content of the SR; (2) the properties of the SR Ca release channel or ryanodine receptor (RyR); (3) the amplitude of the L-type Ca current. The data reviewed show that the Ca content of the SR has pronounced effects on systolic [Ca2+]i and, reciprocally, the amount of Ca released from the SR affects sarcolemmal Ca fluxes thereby "autoregulating" SR content. Modulation of the ryanodine receptor has no steady-state effect due to compensating changes of SR Ca content. An increase of the L-type Ca current results in an abrupt increase of systolic [Ca2+]i with little change of SR content. This is because of a coordinated increase of both the trigger and loading function of the Ca current. These results emphasise the importance of considering all aspects of Ca handling in the context of SR Ca release and thus the regulation of the systolic Ca transient and contraction in cardiac muscle.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Frontiers in bioscience : a journal and virtual library
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
