TRP Channels: Emerging Links Between Ca2+, Kidney and Hypertension
Cationic channels with variable selectivity for Ca2+, K+, and Na+ are ubiquitous in non-excitable tissues as well
as contractile cardiac cells and vascular smooth muscle (VSMC). They are involved in multiple cell functions, including
contraction and proliferation of VSMC, key to the regulation of vascular tone and blood pressure. A large superfamily
includes at least 28 highly conserved heterotetramer homologues of Drosophila TRP (transient receptor potential)
channels. Direct evidence exists for TRPC, TRPV, TRPP gating ion entry in vascular cells, as well as in epithelial cells of
kidney and intestine, thus controlling homeostasis and external balance of divalent cations. Mice deficient in TRPV5
display phenotypic defects resembling human idiopathic hypercalciuria and impaired bone mineral density. Polycystin 2,
encoded by the PKD2 gene, is an epithelial transmembrane TRPP2 protein, whose mutation is associated with autosomal
dominant polycystic kidney disease (ADPKD). TRP ion channels may therefore play a role in the pathogenesis of
systemic arterial hypertension, pulmonary hypertension, as well as hypertension complicating renal disease via effects on
vascular tone and/or on the electrolyte composition of body fluids.
Keywords: Transient Receptor Potential Channels, Store-Operated Ca2+ entry, Pulmonary Hypertension, Arterial
Hypertension, photoreceptors, TRP channels, vasorelaxant agents, hypertensive congenital disorders, endothelial cells.
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