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This review describes the molecular characteristics, biophysical and pharmacological profiles, and functional involvement of T-type calcium channels (Cav3.1) in pulmonary microvascular endothelial cells.
This review summarizes the molecular, biophysical, and pharmacological profiles of T-type calcium channels (Cav3.1) in pulmonary microvascular endothelial cells.
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No immediate clinical implications for pulmonary vascular disease; leaves open Cav3.1 as a potential target pending interventional studies.
The expression of low-voltage-gated T-type calcium channel alpha1G-subunit (Cav3.1) has recently been revealed in pulmonary microvascular endothelial cells (PMVECs). In endothelial cells, changes in membrane potential may be caused by a variety of physiological or pathophysiological vascular stimuli. Thus, the characteristic low-voltage range of activation, transient kinetics of inactivation, and conducting continuous Ca2+ entry in a range of low membrane potentials of this channel may confer its temporal and spatial control of cytosolic Ca2 + important for a variety of cellular processes in vascular endothelial cells. The goal of this review is to provide a succinct description of the endothelial cell T-type calcium channel, including its molecular characteristics, biophysical and pharmacological profiles, and involvement in certain endothelial cell functions.
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Zhou et al. (2006) reported a review. T-type calcium channels (Cav3.1) was evaluated. This review describes the molecular characteristics, biophysical and pharmacological profiles, and functional involvement of T-type calcium channels (Cav3.1) in pulmonary microvascular endothelial cells.
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