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Abstract
Voltage-gated Na+ channels consist of a large alpha subunit of 260 kDa associated with beta 1 and/or beta 2 subunits of 36 and 33 kDa, respectively. alpha subunits of rat cardiac Na+ channels (rH1) are functional when expressed alone in Xenopus oocytes or mammalian cells. beta 1 subunits are present in the heart, and localization of beta 1 subunit mRNA by in situ hybridization shows expression in the perinuclear cytoplasm of cardiac myocytes. Coexpression of beta 1 subunits with rH1 alpha subunits in Xenopus oocytes increases Na+ currents up to 6-fold in a concentration-dependent manner. However, no effects of beta 1 subunit coexpression on the kinetics or voltage dependence of the rH1 Na+ current were detected. Increased expression of Na+ currents is not observed when an equivalent mRNA encoding a nonfunctional mutant beta 1 subunit is coexpressed. Our results show that beta 1 subunits are expressed in cardiac muscle cells and that they interact with alpha subunits to increase the expression of cardiac Na+ channels in Xenopus oocytes, suggesting that beta 1 subunits are important determinants of the level of excitability of cardiac myocytes in vivo.
Highlights
Cardiac Naϩ channels are responsible for the rapid, depolarizing upstroke in the cardiac action potential
We have investigated whether 1 subunit mRNA is expressed in cardiac muscle cells using in situ hybridization, and we have examined the functional role of 1 subunits in modulating cardiac Naϩ channel expression and kinetics by coexpression of mRNA for ␣ and 1 subunits in Xenopus oocytes
We report that 1 subunit mRNA is expressed in cardiac muscle cells in vivo
Summary
Cardiac Naϩ channels are responsible for the rapid, depolarizing upstroke in the cardiac action potential. Currents due to brain or skeletal muscle Naϩ channel ␣ subunits expressed alone by injection of mRNA in Xenopus oocytes are small and have abnormally slow kinetics (Auld et al, 1988; Krafte et al, 1988; Joho et al, 1990; Krafte et al, 1990).
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