Ions, parathyroids, and genetic hypertension

Several reports suggested an involvement of parathyroid function in blood pressure regulation in animals and humans: hyperparathyroid subjects frequently display an elevated systolic blood pressure and young mild hypertensive patients show enhanced serum PTH levels. Moreover, removal of parathyroid glands (PTX) in young rats attenuates and delays the development of mineralocorticoid and genetic hypertension. In addition, in vivo cardiovascular reactivity to norepinephrine in PTX rats from both spontaneously the hypertensive rat (SHR) and Lyon hypertensive rat (LH) strains is decreased, as is calcium content in aortic and heart fragments. Moreover, parathyroid grafts from SHR, stroke-prone SHR (SHR-SP), LH, or Milan hypertensive rats (MHS) into previously parathyroidectomized normotensive recipient rats have been shown to induce an increase in blood pressure. Recently, in essential hypertensive patients and in SHR, a circulating hypertensive factor has also been described. Produced by the PTX in SHR, this factor is inversely related to the amount of dietary calcium. It appears, therefore, that the PTX plays a major role in experimental and probably also in human hypertension.