Pang P K, Benishin C G, Shan J, Lewanczuk R Z
Department of Physiology, University of Alberta, Edmonton, Canada.
Blood Press. 1994 May;3(3):148-55. doi: 10.3109/08037059409102245.
Parathyroid Hypertensive Factor (PHF) was discovered in SHR rats as a circulating substance with a unique delayed (60-90 min) hypertensive effect when injected into a normotensive assay rat. Subsequently, this correlation with hypertension was established in humans, especially in low-renin, salt-sensitive patients. Animal model studies also confirmed this correlation. Endocrinectomy and glandular replacement studies suggested that the parathyroid gland was the source of PHF. Subsequently, glands and cells in culture were also shown to secrete the substance. Other studies verified the parathyroid origin of PHF. The mechanism of action of PHF was shown to rely mainly on the opening of L-type calcium channels in vascular smooth muscle cells with an increase in [Ca2++]i. It is known that diseases other than hypertension often show increased [Ca2++]i and clinical features similar to hypertension, among them Type II diabetes. A recent study shows a correlation between circulating PHF level and Type II diabetes irrespective of the blood pressure status of the patient. It is suggested that PHF may be a [Ca++]i modulator, an excessive amount of which in the circulation may act on various target tissues, resulting in various disease symptoms with hypertension as an example. There may be many other such PHF-related diseases yet to be identified.
甲状旁腺高血压因子（PHF）是在自发性高血压大鼠（SHR）中发现的一种循环物质，当将其注入血压正常的实验大鼠体内时，会产生独特的延迟（60 - 90分钟）高血压效应。随后，在人类中也证实了这种与高血压的关联，尤其是在低肾素、盐敏感患者中。动物模型研究也证实了这种关联。内分泌切除和腺体替代研究表明甲状旁腺是PHF的来源。随后，培养中的腺体和细胞也被证明能分泌这种物质。其他研究证实了PHF的甲状旁腺起源。PHF的作用机制主要依赖于血管平滑肌细胞中L型钙通道的开放以及细胞内钙离子浓度（[Ca2 +]i）的增加。已知除高血压外的其他疾病也常常表现出细胞内钙离子浓度升高以及与高血压相似的临床特征，其中包括II型糖尿病。最近的一项研究表明，无论患者的血压状况如何，循环中的PHF水平与II型糖尿病之间都存在关联。有人提出，PHF可能是一种细胞内钙离子浓度调节剂，循环中过量的PHF可能作用于各种靶组织，导致以高血压为例的各种疾病症状。可能还有许多其他此类与PHF相关的疾病有待发现。
