AJP - Gastrointestinal and Liver Physiology, Vol 260, Issue 5 691-G697, Copyright © 1991 by American Physiological Society
Intestinal vitamin D-dependent calbindin-D9k and alkaline phosphatase in spontaneously hypertensive rats
D. L. Cloney, R. W. Gray, M. E. Bruns, S. H. Burnett, M. L. Smith, R. A. Felder and D. E. Bruns
Department of Pathology, University of Virginia School of Medicine, Charlottesville 22908.
Intestinal Ca2+ malabsorption has been described in spontaneously
hypertensive rats (SHRs), but the molecular basis for this defect is
unknown. In this study, we measured intestinal alkaline phosphatase and
vitamin D-dependent Ca(2+)-binding protein (calbindin-D9k), two proteins
implicated in the active pathway of intestinal Ca2+ absorption. Both
proteins were measured in the small intestines of SHRs and their
normotensive controls, Wistar-Kyoto rats, before, during, and after
development of hypertension (4, 9, 14, 18, and 28 wk of age). At all ages,
alkaline phosphatase activity in duodenum (0-6 cm) was decreased by 30-57%
(P less than 0.001) and by 47-75% in the 2nd intestinal segment (6-12 cm)
(P less than 0.001-0.05). Calbindin-D9k was decreased similarly. The
decreases of calbindin were statistically significant (P less than
0.001-0.05) in the duodena at 4, 14, 18, and 28 wk (9-30% decreases) and in
the 2nd segment at 4, 14, and 18 wk (38-69% decreases; P less than
0.001-0.005). Decreased calbindin in SHRs was documented in animals from
two suppliers. The deficiencies of calbindin-D9k and alkaline phosphatase
could not be attributed to malnutrition or to a generalized brush-border
defect as indicated by body weights and the intestinal marker enzyme
sucrase. Although calbindin-D9k was decreased in young SHRs, the serum
1,25-dihydroxycholecalciferol [1,25(OH)2D3] was increased by 59 and 129% in
4- and 9-wk-old SHRs (P less than 0.001), respectively; by contrast, serum
1,25(OH)2D3 was unchanged or decreased in older SHRs.(ABSTRACT TRUNCATED AT
250 WORDS)
