Literature DB >> 8275530

The relative contributions of different intracellular and sarcolemmal systems to relaxation in rat ventricular myocytes.

N Negretti1, S C O'Neill, D A Eisner.   

Abstract

OBJECTIVE: The aim was to estimate the relative contributions of the various intracellular and sarcolemmal systems to the relaxation of the systolic calcium transient.
METHODS: The experiments were performed on isolated rat ventricular myocytes. The cells were loaded with the fluorescent indicator indo-1 in order to measure [Ca2+]i.
RESULTS: The application of caffeine to release calcium from the sarcoplasmic reticulum produced a rise of [Ca2+]i which decayed about 7-8 times more slowly than the electrically stimulated calcium transient. This suggests that the sarcoplasmic reticulum accounts for about 87% of the calcium removal. The rate of decay of the caffeine response was decreased to about 33% of the control by inhibiting the Na-Ca exchange with Ni2+. In the presence of Ni2+ the rate could be inhibited further by inhibiting either the sarcolemmal Ca-ATPase (by increasing extracellular calcium concentration, [Ca2+]o) or the mitochondria (with FCCP and oligomycin). The relative contributions of the various processes were estimated to be: sarcoplasmic reticulum 87%, mitochondria 1.7%, Na-Ca 8.7%, sarcolemmal Ca-ATPase 2.6%.
CONCLUSIONS: These experiments show that the Na-Ca exchange accounts for 67% of the calcium removal not mediated by the sarcoplasmic reticulum. This is a smaller fraction than in rabbit cardiac cells and highlights the importance of the Ca-ATPase in the rat heart.

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Year:  1993        PMID: 8275530     DOI: 10.1093/cvr/27.10.1826

Source DB:  PubMed          Journal:  Cardiovasc Res        ISSN: 0008-6363            Impact factor:   10.787


  47 in total

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2.  Paradoxical block of the Na+-Ca2+ exchanger by extracellular protons in guinea-pig ventricular myocytes.

Authors:  M Egger; E Niggli
Journal:  J Physiol       Date:  2000-03-01       Impact factor: 5.182

3.  A computational model of cytosolic and mitochondrial [ca] in paced rat ventricular myocytes.

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4.  Modulation of CICR has no maintained effect on systolic Ca2+: simultaneous measurements of sarcoplasmic reticulum and sarcolemmal Ca2+ fluxes in rat ventricular myocytes.

Authors:  A W Trafford; M E Díaz; G C Sibbring; D A Eisner
Journal:  J Physiol       Date:  2000-01-15       Impact factor: 5.182

5.  The calcium-frequency response in the rat ventricular myocyte: an experimental and modelling study.

Authors:  Sara Gattoni; Åsmund Treu Røe; Michael Frisk; William E Louch; Steven A Niederer; Nicolas P Smith
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Review 6.  Why don't mice lacking the mitochondrial Ca2+ uniporter experience an energy crisis?

Authors:  Pei Wang; Celia Fernandez-Sanz; Wang Wang; Shey-Shing Sheu
Journal:  J Physiol       Date:  2018-10-11       Impact factor: 5.182

7.  Negative inotropic effects of tumour necrosis factor-alpha and interleukin-1beta are ameliorated by alfentanil in rat ventricular myocytes.

Authors:  D J Duncan; P M Hopkins; S M Harrison
Journal:  Br J Pharmacol       Date:  2007-02-05       Impact factor: 8.739

8.  Regional differences in rest decay and recoveries of contraction and the calcium transient in rabbit ventricular muscle.

Authors:  J P Chamunorwa; S C O'Neill
Journal:  Pflugers Arch       Date:  1995-06       Impact factor: 3.657

9.  Steady-state coupling of plasma membrane calcium entry to extrusion revealed by novel L-type calcium channel block.

Authors:  William C Lester; Elizabeth A Schroder; Don E Burgess; Doug Yozwiak; Douglas A Andres; Jonathan Satin
Journal:  Cell Calcium       Date:  2008-10       Impact factor: 6.817

10.  Estimate of net calcium fluxes and sarcoplasmic reticulum calcium content during systole in rat ventricular myocytes.

Authors:  N Negretti; A Varro; D A Eisner
Journal:  J Physiol       Date:  1995-08-01       Impact factor: 5.182

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