Disturbances of calcium metabolism in experimental hypertension.

The metabolism of Ca2+ is profoundly disturbed in the spontaneously hypertensive rat (SHR), compared with its normotensive control, the Wistar-Kyoto rat. This is true for the whole animal as well as at the cellular and the subcellular level. Many apparently discrepant results of the literature could be due to differences in age, gender, strain, and type of diet. It is possible that the SHR has initially an epithelial (and a nonepithelial) Ca2+ transport defect. This could in turn lead to a more or less efficient stimulation of calcitriol synthesis and a compensatory increase in calcium absorption during early life. With the maturation of the animal, however, a state of calcium and vitamin D deficiency would prevail. In this scheme, the observed defect of epithelial Ca2+ transport in the SHR is primary in nature, reflecting some perturbation of Ca2+ handling by the cell, and the changes of vitamin D metabolism and hyperparathyroidism are secondary. Altered cellular Ca2+ permeability and a compromised ability of the cell to remove or sequester Ca2+ may be relevant to the pathogenesis and maintenance of hypertension. Parathyroid gland overfunction and vitamin D deficiency may also be involved in the elevation of arterial pressure. Our knowledge of such interactions is however still incomplete. Much more has to be learnt about the probable link between alterations of Ca2+ metabolism and elevated blood pressure.