Schleiffer R
CNRS UA600, Faculté de Pharmacie, U. Louis Pasteur Strasbourg, Illkirch, France.
J Endocrinol Invest. 1992;15(9 Suppl 6):87-95.
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.
尽管甲状旁腺激素（PTH）在生长激素受体（GHR）中的精确机制尚未完全明了，但迄今为止的研究与GHR模型中继发性甲状旁腺功能亢进的存在相符。由于肾钙泄漏和/或肠道钙吸收不足导致的低血清离子钙水平应是PTH分泌过多的刺激因素。长期口服钙剂或切除甲状旁腺均可预防和减轻遗传性高血压的发展，这一事实支持了该假说。得出的结论是，PTH可能与维生素D或甲状旁腺高血压因子等其他因素共同作用，在GHR高血压的发生和维持中起允许作用。
