Triggering of sarcoplasmic reticulum [Ca.sup.2+] release and contraction by reverse mode [Na.sup.+]/[Ca.sup.2+] exchange in trout atrial myocytes

Whole cell patch clamp and intracellular [Ca.sup.2+] transients in trout atrial cardiomyocytes were used to quantify calcium release from the sarcoplasmic reticulum (SR) and examine its dependency on the [Ca.sup.2+] trigger source. Short depolarization pulses (2-20 ms) elicited large caffeine-sensitive tail currents. The [Ca.sup.2+] carried by the caffeine-sensitive tail current after a 2-ms depolarization was 0.56 amol [Ca.sup.2+]/pF, giving an SR [Ca.sup.2+] release rate of 279 amol [Ca.sup.2+]*[p.sup.F-1]* [s.sup.-1] or 4.3 mM/s. Depolarizing cells for 10 ms to different membrane potentials resulted in a local maximum of SR [Ca.sup.2+] release, intracellular [Ca.sup.2+] transient, and cell shortening at 10 reV. Although 100 [micro]M CD[Cl.sub.2] abolished this local maximum, it had no effect on SR [Ca.sup.2+] release elicited by a depolarization to 110 or 150 reV, and the SR [Ca.sup.2+] release was proportional to the membrane potential in the range -50 to 150 mV with 100 [micro]M CD[Cl.sub.2]. Increasing the intracellular [Na.sup.+] concentration ([Na.sup.+]) from 10 to 16 mM enhanced SR [Ca.sup.2+] release but reduced cell shortening at all membrane potentials examined. In the absence of TTX, SR [Ca.sup.2+] release was potentiated with 16 mM but not 10 mM pipette [Na+]. Comparison of the total sarcolemmal [Ca.sup.2+] entry and the [Ca.sup.2+] released from the SR gave a gain factor of 18.6 [- or +] 7.7. Nifedipine (Nil) at 10 [micro]M inhibited L-type [Ca.sup.2+] current ([I.sub.ca]) and reduced the time integral of the tail current by 61%. The gain of the Nif-sensitive SR [Ca.sup.2+] release was 16.0 [+ or -] 4.7. A 2-ms depolarization still elicited a contraction in the presence of Nif that was abolished by addition of 10 mM Ni[Cl.sub.2]. The gain of the Nilinsensitive but Ni[Cl.sub.2]-sensitive SR [Ca.sup.2+] release was 14.8 [+ or -] 7.1. Thus both reverse-mode [Na.sup.+]/[Ca.sup.2+] exchange (NCX) and [I.sub.ca] can elicit [Ca.sup.2+] release from the SR, but [I.sub.ca] is more efficient than reverse-mode NCX in activating contraction. This difference may be due to extrusion of a larger fraction of The [Ca.sup.2+] released from the SR by reverse-mode NCX rather than a smaller gain for NCX-induced [Ca.sup.2+] release. [Ca.sup.2+] current; [Ca.sup.2+] transients; caffeine; cardiac; excitation-contraction coupling