This study provides the first evidence of Nav1.4 expression in human esophageal smooth muscle cells, contributing to the understanding of excitation in these cells.
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Hypothesis-generating for esophageal ion channel physiology; leaves open any role in motility disorders pending in vivo studies.
Smooth muscle contraction is critical to peristalsis in the human esophagus, yet the nature of the channels mediating excitation remains to be elucidated. The objective of this study was to characterize the inward currents in human esophageal smooth muscle cells (HESMCs). Esophageal tissue was isolated from patients undergoing surgery for cancer and grown in primary culture, and currents were recorded using patch-clamp electrophysiology. Depolarization elicited inward current activating positive to -40 mV and peaking at 0 mV and consisting of transient and sustained components. The transient current was half activated at -16 mV and half inactivated at -67 mV. The transient current was abolished by removal of bath Na(+) or application of TTX (IC(50) ~20 nM), whereas it persisted in the absence of bath Ca(2+) or the presence of Cd(2+). These data provide evidence that cultured HESMCs express voltage-dependent Na(+) channels. RT-PCR revealed mRNA transcripts for Na(x), the "atypical" Na(+) channel isoform, as well as Na(v)1.4. These studies provide the first evidence of Na(v)1.4 in smooth muscle and contribute to a model of excitation in HESMCs.
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Deshpande et al. (2002) studied this question.
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