CELLULAR CALCIUM ION UPTAKE AND EXTRACELLULAR (CALCIUM ION) DEPLETION IN FROG VENTRICULAR MUSCLE.
Item
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Title
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CELLULAR CALCIUM ION UPTAKE AND EXTRACELLULAR (CALCIUM ION) DEPLETION IN FROG VENTRICULAR MUSCLE.
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Identifier
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AAI8401928
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identifier
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8401928
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Creator
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DRESDNER, KARL P., JR.
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Contributor
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Richard P. Kline
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Date
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1983
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Language
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English
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Publisher
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City University of New York.
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Subject
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Health Sciences, Pharmacology
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Abstract
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The extracellular calcium ion concentration ({lcub}Ca('++){rcub}(,0)) in contracting frog ventricular myocardium was directly and continuously measured with a Ca('++) selective microelectrode (Ca-ISE). Frog (Rana pipiens) ventricular strips were superfused with 0.050 to 0.20 millimolar Ca('++) Ringers to reduce muscle contraction. A few experiments were successful in higher Ca('++) Ringers. For some positions of the Ca-ISE tip, the {lcub}Ca('++){rcub}(,0) significantly decreased during the action potential. As fast repolarization of the membrane potential occurred, the depletion of {lcub}Ca('++){rcub}(,0) stopped. Following repolarization, the {lcub}Ca('++){rcub}(,0) increased rapidly toward baseline suggesting that the tip of the Ca-ISE was positioned in the small clefts surrounding the cells. At other Ca-ISE tip locations (presumably in larger clefts), the beat to beat {lcub}Ca('++){rcub}(,0) fluctuations were small or absent.;We estimated the Ca('++) flux/cm('2) cell membrane required to generate depletion. The estimated increase in the intracellular {lcub}Ca('++){rcub} which would result from the transmembrane Ca('++) influx was 0.5 to 8.8 micromoles per liter cells (with 0.050 to 1.0 Ca('++) Ringers). This is comparable to the quantity of Ca('++) required to catalyze muscle contracton.;During acute increase in the stimulation rate, the {lcub}Ca('++){rcub}(,0) fell in 3 to 5 minutes to a minimum level. The minimum {lcub}Ca('++){rcub}(,0) was attained sooner when the {lcub}Ca('++){rcub}(,0) depletion was large, indicating that cellular Ca('++) uptake turned off as the transmembrane {lcub}Ca('++){rcub} gradient was dissipated. {lcub}Ca('++){rcub}(,0) depletion during repetitive stimulation was enhanced in low Na('+) Ringers and reduced by manganese or nickel ions. Catecholamines increased the rate and magnitude of {lcub}Ca('++){rcub}(,0) depletion and were blocked by propranolol, nickel, or manganese ions. Contracture fluid (high K('+)/low Na('+) Ringers) caused significant {lcub}Ca('++){rcub}(,0) depletion. When interventions prolonged {lcub}Ca('++){rcub}(,0) depletion beyond 4 minutes a cellular efflux of Ca('++) was activated which caused a prolonged postdrive overshoot of {lcub}Ca('++){rcub}(,0).
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Type
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dissertation
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Source
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PQT Legacy CUNY.xlsx
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degree
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Ph.D.
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Program
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Biomedical Sciences
