Bimodal effect of stimulation on light fluctuation transients monitoring spontaneous sarcoplasmic reticulum calcium release in rat cardiac muscle.
Microscopic, myofilament motion caused by spontaneous oscillatory Ca2+ release from the sarcoplasmic reticulum (SR) of unstimulated rat papillary muscles produces scattered light intensity fluctuations (SLIF) in a laser beam scattered by the tissue. SLIF frequency increases with Ca2+ loading of resting muscle. We used novel time-gated SLIF measurements to determine how electrical stimulation (which per se both induces SR Ca2+ release and modulates total cellular Ca2+ loading) affects SLIF. Stimulation of thin rat, right ventricular muscles at 1 Hz in bathing [Ca2+] (Ca0) of 1.5 mM at 29 degrees C abolished SLIF for 5-7 seconds; SLIF then reappeared and monotonically increased for 10-15 seconds to reach the steady resting level. Resting force transients paralleled those of SLIF. The magnitude of depression and time course of recovery of both resting force and SLIF at this Ca0 vary inversely with the rate of prior stimulation and the number of stimuli given. An increase in Ca0 or disablement of the Na-K pump increased both resting SLIF and force; transient stimulation under these conditions (i.e., in a 2.5-5.5-second "diastolic window" after cessation of stimulation) augmented SLIF and force above the resting level. Isoproterenol caused a modest reduction of resting SLIF, but it transiently increased SLIF after stimulation up to 10-fold above the resting level. Nifedipine did not affect resting SLIF but transiently depressed SLIF after stimulation. Ryanodine abolished SLIF both after stimulation and at rest.(ABSTRACT TRUNCATED AT 250 WORDS)
- Copyright © 1988 by American Heart Association