Importance of 25-Hydroxylation to the Renal Tubular Actions of Vitamin D Metabolites

Abstract

Experimental observations from my own laboratory as well as data from other workers have documented an acute effect of vitamin D and certain of its metabolites on renal tubular electrolyte transport (1–5). Both in the dog and the rat, the infusion of the biologically active derivative of vitamin D₃, 25-hydroxycholecalciferol (25 HCC) and 1,25-dihydroxycholecalciferol (1,25 DHCC) has been demonstrated to produce an acute enhancement of phosphate (1–5), calcium and sodium (4,5) reabsorption. Recently, a series of additional metabolites and analogues has been discovered (6). Their subsequent characterization and synthesis have provided us with the opportunity to study the structural requirements of these vitamin D₃ derivatives with regard to their ability to alter renal tubular transport. The protocol utilized for these studies was identical to that originally described (1).