AJP - Gastrointestinal and Liver Physiology, Vol 248, Issue 6 676-G681, Copyright © 1985 by American Physiological Society
Effects of 1,25(OH)2D3 and calcium channel blockers on cecal calcium transport in the rat
M. J. Favus and E. Angeid-Backman
To determine whether calcium transport across rat cecum is vitamin D
dependent, we measured in vitro bidirectional calcium fluxes under
short-circuited conditions across cecum from rats that were vitamin D
deficient, vitamin D replete, or vitamin D deficient or vitamin D replete
and injected with either 10, 25, or 75 ng of 1,25-dihydroxyvitamin D3
[1,25(OH)2D3] daily for 4 days before study. Vitamin D deficiency decreased
net calcium absorption (Jnet) by reducing the mucosal-to-serosal absorptive
flux (Jm----s) from 168 +/- 18 to 33 +/- 5 nmol X cm-2 X h-1 (mean +/- SE,
P less than 0.0001). Twenty-five nanograms of 1,25(OH)2D3 raised Jm----s to
124 +/- 17 nmol X cm-2 X h-1, not different from values in vitamin
D-replete rats. Although active calcium absorption by cecum appears to
respond to vitamin D, calcium Jm----s is near maximal under normal
conditions, and further stimulation follows only pharmacological doses of
1,25(OH)2D3. The in vitro addition of the calcium channel blocker verapamil
(5 X 10(-5) M) to the mucosal side of cecum from vitamin D-replete rats
reduced calcium Jm----s, but lower concentrations of verapamil or
nitrendipine (10(-5) to 10(-9) M) did not reduce calcium Jm----s. The lack
of inhibition by low concentrations of channel blockers suggest that the
plasma membrane channels for calcium translocation across intestinal
epithelium may not be analogous to voltage-dependent calcium channels in
excitable tissue. The inhibition of cecal calcium transport that was
blocked by high concentrations of verapamil may represent a nonspecific
effect of the agent.
