Literature DB >> 9614497

Contribution of reverse-mode sodium-calcium exchange to contractions in failing human left ventricular myocytes.

J A Mattiello1, K B Margulies, V Jeevanandam, S R Houser.   

Abstract

OBJECTIVE: To examine the contribution of reverse mode sodium-calcium (Na-Ca) exchange to contractions in isolated left-ventricular myocytes from failing human heart.
METHODS: Low resistance patch pipettes were used to dialyze cells with Na-free or high-Na pipette solution ([Na]pipette = 0 and 20 mmol/L, respectively) to reduce or enhance Na-Ca exchange. Whole-cell membrane-potential, membrane-current and cell-shortening data were simultaneously acquired during whole-cell voltage clamp protocols. Thapsigargin (100 nmol/L) and nifedipine (1 mumol/L) were also used to inhibit sarcoplasmic reticulum (SR) Ca-ATPase and L-type Ca channels, respectively.
RESULTS: Two types of contractions were observed. Rapid phasic contractions were seen in both Na-free and high-Na cells. Slow tonic contractions were seen only in high-Na cells. Phasic contractions demonstrated bell-shaped voltage dependence over the voltage range that corresponds to the activity of the L-type Ca channel. Although the voltage dependence of phasic contractions were similar Na-free and high-Na cells, phasic contractions in high-Na cells were larger than phasic contractions in Na-free cells. Phasic contractions were sensitive to inhibition of SR Ca-ATPase and L-type Ca channels. Tonic contractions were not inhibited by either thapsigargin or nifedipine. In thapsigargin-treated high-Na cells, tonic contraction magnitude increased exponentially with test-potential.
CONCLUSIONS: The increases in phasic contraction magnitude observed in high-Na cells compared to Na-free cells were most likely due to increased SR Ca loading resulting from increased reverse-mode Na-Ca exchange. Our results also suggest that tonic contractions in high-Na cells were mediated by Ca entry via reverse-mode Na-Ca exchange and were not the result of either SR Ca release or L-type Ca channel activity.

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Year:  1998        PMID: 9614497     DOI: 10.1016/s0008-6363(97)00271-x

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


  14 in total

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