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PMID: 3783123 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Relationships between the sarcoplasmic reticulum and sarcolemmal calcium transport revealed by rapidly cooling rabbit ventricular muscle.

The Journal of general physiology ·Vol. 88 ·No. 4 ·1986-10-00 ·Pages 437-73

Bridge JH

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.

MeSH Terms
Animals Biological Transport Caffeine/pharmacology Calcium/metabolism,physiology Cold Temperature Fourier Analysis In Vitro Techniques Membrane Potentials Myocardial Contraction/drug effects Myocardium/metabolism Rabbits Sarcolemma/metabolism Sarcoplasmic Reticulum/metabolism Strophanthidin/pharmacology Time Factors
Chemicals
Caffeine Strophanthidin Calcium
Authors & Affiliations
1 authors, click to expand affiliations / ORCID
Bridge J H
Article Info
Journal
The Journal of general physiology
Abbr.
J Gen Physiol
ISSN
0022-1295
Published
1986-10-00
Pages
437-73
Language
English
Region
United States
NLM ID
2985110R
PMCID
PMC2228846
Subset
IM
Grants
NHLBI NIH HHS · HL 13340 · United States
NHLBI NIH HHS · HL 13480 · United States
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