AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 274: H155-H170, 1998;
0363-6135/98 $5.00
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Vol. 274, Issue 1, H155-H170, January 1998

Contribution of a voltage-sensitive calcium release mechanism to contraction in cardiac ventricular myocytes

Susan E. Howlett, Jie-Quan Zhu, and Gregory R. Ferrier

Cardiovascular Research Laboratories, Department of Pharmacology, Dalhousie University, Halifax, Nova Scotia, Canada B3H 4H7

The contribution of a voltage-sensitive release mechanism (VSRM) for sarcoplasmic reticulum (SR) Ca2+ to contraction was investigated in voltage-clamped ventricular myocytes at 37°C. Na+ current was blocked with lidocaine. The VSRM exhibited steady-state inactivation (half-inactivation voltage: -47.6 mV; slope factor: 4.37 mV). When the VSRM was inactivated, contraction-voltage relationships were proportional to L-type Ca2+ current (ICa-L). When the VSRM was available, the relationship was sigmoidal, with contractions independent of voltage positive to -20 mV. VSRM and ICa-L contractions could be separated by activation-inactivation properties. VSRM contractions were extremely sensitive to ryanodine, thapsigargin, and conditioning protocols to reduce SR Ca2+ load. ICa-L contractions were less sensitive. When both VSRM and ICa-L were available, sigmoidal contraction-voltage relationships became bell-shaped with protocols to reduce SR Ca2+ load. Myocytes demonstrated restitution of contraction that was slower than restitution of ICa-L. Restitution was a property of the VSRM. Thus activation and recovery of the VSRM are important in coupling cardiac contraction to membrane potential, SR Ca2+ load, and activation interval.

excitation-contraction coupling; calcium current; cardiac muscle; sarcoplasmic reticulum; ryanodine


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