| pubmed-article:1352089 | pubmed:abstractText | Recent studies from our laboratory have demonstrated that the in vitro addition of 1,25-dihydroxycholecalciferol [1,25(OH)2D3] rapidly (seconds to minutes) stimulated membrane phosphoinositide turnover, translocated protein kinase C from the cytosolic to particulate fraction, increased cytosolic calcium ([Ca2+]i), and decreased cytoplasmic pH (pHi) via inhibition of Na(+)-H+ exchange in rat colonic epithelium of dietary vitamin D-sufficient rats and in Caco-2 cells. In contrast to these prior findings, in the present experiments, 1,25(OH)2D3 failed to elicit any of these colonic biochemical responses in vitamin D-deficient animals. Bethanechol chloride also failed to alter this signal transduction pathway, [Ca2+]i, or pHi. In vivo administration of this hormone for 5-7 days, moreover, to vitamin D-deficient animals restored the rapid biochemical effects of in vitro 1,25(OH)2D3 and bethanechol chloride. These studies, therefore, indicate that alterations in the vitamin D status of rats modulate the action of 1,25(OH)2D3 and other agents on the colonic phosphoinositide signal transduction system and on [Ca2+]i, which, in turn, may influence important cellular processes in this organ such as Na(+)-H+ exchange. | lld:pubmed |
