Author:

Keywords:

Animals, Calcium, Calcium Channels, Epithelial Cells, Humans, Metabolic Diseases, Research Support, Non-U.S. Gov't, TRPV Cation Channels, Science & Technology, Life Sciences & Biomedicine, Physiology, calcium transport, ECaC1, ECaC2, estrogen, hypercalciuria, vitamin D, INTESTINAL CALCIUM-ABSORPTION, HUMAN PROSTATIC-CARCINOMA, DISTAL CONVOLUTED TUBULE, RAT PANCREATIC-ISLETS, SENSING RECEPTOR GENE, NA+-CL COTRANSPORTER, VITAMIN-D, IDIOPATHIC HYPERCALCIURIA, SODIUM-TRANSPORT, RENAL CALCIUM, 0606 Physiology, 1106 Human Movement and Sports Sciences, 1116 Medical Physiology, 3101 Biochemistry and cell biology, 3109 Zoology, 3208 Medical physiology

Abstract:

The epithelial Ca(2+) channels TRPV5 and TRPV6 constitute the apical Ca(2+) entry mechanism in active Ca(2+) (re)absorption. These two members of the superfamily of transient receptor potential (TRP) channels were cloned from the vitamin-D-responsive epithelia of kidney and small intestine and subsequently identified in other tissues such as bone, pancreas and prostate. These channels are regulated by vitamin D as exemplified in animal models of vitamin-D-deficiency rickets. In addition, the epithelial Ca(2+) channels might be involved in the multifactorial pathogenesis of disorders ranging from idiopathic hypercalciuria, stone disease and postmenopausal osteoporosis. This review highlights the emerging (patho)physiological implications of these epithelial Ca(2+) channels.