Abnormal regulation of intestinal calbindin (CaBP9k) and calmodulin in the spontaneously hypertensive rat.

This review focuses particularly on abnormalities of Ca-binding proteins in transporting epithelia, which have been observed in various models of experimental hypertension. The enterocyte content of integral membrane Ca(2+)-binding protein (IMCAL) and calbindin-9k and the renal tubular calbindin-28k content have been shown to be decreased in the spontaneously hypertensive rat (SHR), compared with normotensive control rats (WKY). Similarly, calmodulin content was decreased in several tissues including the intestine; however, calmodulin activity was increased. In recent studies, the authors examined the response of intestinal calbindin-9k, calbindin-9k mRNA, and calmodulin contents to low-Ca and high-Ca diets in these two rat strains. It was shown that the SHR, unlike the WKY, was unable to augment intestinal calbindin-9k and calbindin-9k mRNA levels in response to a low-Ca diet of short duration. On the other hand, a high-Ca diet led to a similar decrease in calbindin-9k content in both SHR and WKY rats. Enterocyte calmodulin content was also diminished in the WKY, but not the SHR, fed such a high-Ca diet. Therefore, abnormal Ca-binding proteins could play a role in the disturbed Ca metabolism of arterial hypertension.