Relationships between the sarcoplasmic reticulum and sarcolemmal calcium transport revealed by rapidly cooling rabbit ventricular muscle.
Open Access
- 30 September 1986
- journal article
- research article
- Published by Rockefeller University Press in The Journal of general physiology
- Vol. 88 (4), 437-473
- https://doi.org/10.1085/jgp.88.4.437
Abstract
Rabbit right ventricular papillary muscles were cooled from 30 to approximately 1 degree C immediately after discontinuing electrical stimulation (0.5 Hz). This produced a contracture that was 30-50% of the preceding twitch magnitude and required 20-30 s to develop. The contractures were identical in cooling solutions with normal (144 mM) or low (2.0 mM) Na. They were therefore not Na-withdrawal contractures. Contracture activation was considerably slower than muscle cooling (approximately 2.5 s to cool below 2 degrees C). Cooling contractures were suppressed by caffeine treatment (10.0 mM). Rapid cooling did not cause sufficient membrane depolarization (16.5 +/- 1.2 mV after 30 s of cooling) to produce either a voltage-dependent activation of contracture or a gated entry of Ca from the extracellular space. Contractures induced by treating resting muscles with 5 X 10(-5) M strophanthidin at 30 degrees C exhibited pronounced tension noise. The Fourier spectrum of this noise revealed a periodic component (2-3 Hz) that disappeared when the muscle was cooled. Cooling contractures decayed with rest (t1/2 = 71.0 +/- 9.3 s). This decay accelerated in the presence of 10.0 mM caffeine and was prevented and to some extent reversed when extracellular Na was reduced to 2.0 mM. 20 min of rest resulted in a net decline in intracellular Ca content of 1.29 +/- 0.38 mmol/kg dry wt. I infer that cooling contractures are principally activated by Ca from the sarcoplasmic reticulum (SR). The properties of these contractures suggest that they may provide a convenient relative index of the availability of SR Ca for contraction. The rest decay of cooling contractures (and hence the decay in the availability of activating Ca) is consistent with the measured loss in analytic Ca during rest. The results suggest that contraction in heart muscle can be regulated by an interaction between sarcolemmal and SR Ca transport.This publication has 26 references indexed in Scilit:
- Calcium‐activated force responses in fast‐ and slow‐twitch skinned muscle fibres of the rat at different temperatures.The Journal of Physiology, 1981
- The time-course of Ca2+ exchange with calmodulin, troponin, parvalbumin, and myosin in response to transient increases in Ca2+Biophysical Journal, 1981
- The Ca2+-pumping ATPase of heart sarcolemma. Characterization, calmodulin dependence, and partial purification.Journal of Biological Chemistry, 1981
- Calcium transport and contractile activity in dissociated mammalian heart cellsAmerican Journal of Physiology-Cell Physiology, 1979
- Uncoupling cation effects on cardiac contractility and sarcolemmal Ca2+ bindingAmerican Journal of Physiology-Heart and Circulatory Physiology, 1979
- Quantitative ultrastructural analysis in cardiac membrane physiologyAmerican Journal of Physiology-Cell Physiology, 1978
- Two levels of resting potential in cardiac Purkinje fibers.The Journal of general physiology, 1977
- The decay of the potentiated state in sheep and calf ventricular myocardial fibers. Influence of agents acting on transmembrane Ca2+ flux.Circulation Research, 1976
- The dependence of slow inward current in Purkinje fibres on the extracellular calcium‐concentrationThe Journal of Physiology, 1967
- Cat Heart Muscle in Vitro The Journal of general physiology, 1964