Although the precise mechanism(s) of PTH in GHR were not yet fully understood, the research to date is compatible with the presence of a secondary hyperparathyroidism in the GHR models. A low serum ionized calcium level due to renal calcium leak and/or low intestinal absorption of calcium should be the stimulus for PTH hypersecretion. This hypothesis is supported by the fact that both long-term oral calcium supplementation or removal of parathyroid glands prevents and attenuates the development of genetic hypertension. It is concluded that PTH, probably in concomitant with other factors such as vitamin D or parathyroid hypertensive factor, has a permissive effect in the development and the maintenance of hypertension in GHR.