Literature DB >> 10912455

Reexpression of T-type Ca2+ channel gene and current in post-infarction remodeled rat left ventricle.

B Huang1, D Qin, L Deng, M Boutjdir, N E1-Sherif.   

Abstract

OBJECTIVE: T-type Ca2+ currents (I(Ca-T)) are present in neonatal rat myocytes but is not detected in adult ventricular myocytes. The present study was designed to investigate the expression of the T-type Ca2+ channel gene and current in post-infarction remodeled hypertrophied rat left ventricle (LV).
METHODS: We compared the expression of T-type Ca2+ channel gene alpha-1G in neonatal rat LV, in adult sham-operated LV and remodeled hypertrophied LV 3 to 4 weeks post-myocardial infarction (MI) using RNase protection assay (RPA). The cDNA fragment of alpha-1G used in RPA was obtained from poorly conserved region of recently published T-type Ca2+ channel coding sequence of rat by RT-PCR. The fragment was verified by restriction enzyme digestion and sequencing. The presence of I(Ca-T) in LV of sham and post-MI rats was examined using patch-clamp techniques. In the presence of K+-free, Na+-free external solution, I(Ca-T) was separated from I(Ca-L) by different holding potentials (HP). I(Ca-T) was also recorded during depolarization to -40 mV from a HP of -80 mV with NaCl in external solution and I(Na) suppressed by 100 microM tetrodotoxin (TTX).
RESULTS: The T-type Ca2+ channel gene alpha-1G was expressed in neonatal heart, the expression level decreased by 80%, in adult sham heart and was reexpressed in MI (158% increases compared to sham; P<0.01). I(Ca-T) was recorded in 11 of 31 MI cells in presence of K+-free, Na+-free external solution and in 9 of 14 cells when I(Na) was suppressed by TTX. I(Ca-T) was not detected in any of 21 sham cells. I(Ca-T) density was 1.1+/-0.4 pA/pF. I(Ca-T) was more sensitive to Ni2+ and less sensitive to nisoldipine.
CONCLUSIONS: T-type Ca2+ channel gene and current are reexpressed in rat post-MI remodeled LV myocytes. Its functional significance in the post-MI remodeling process remains to be defined.

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Year:  2000        PMID: 10912455     DOI: 10.1016/s0008-6363(00)00017-1

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


  31 in total

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