Campese V M
Department of Medicine, University of Southern California, Los Angeles 90033.
Am J Hypertens. 1989 Feb;2(2 Pt 2):34S-44S. doi: 10.1093/ajh/2.2.34s.
This review critically analyzes the available information on the relationship among calcium, parathyroid hormone, and blood pressure regulation. Both acute and chronic hypercalcemia increase blood pressure primarily via direct effects on vascular smooth muscle contractility. The evidence for indirect effects through activation of hormonal pressor systems is inconclusive. In apparent contrast with the notion that hypercalcemia can cause hypertension, more recently it has been proposed that calcium deficiency may be important in the genesis of hypertension both in humans and in spontaneously hypertensive animals. However, the evidence supporting this notion is still conflicting. Parathyroid hormone exerts complex actions on the cardiovascular system. On one hand, if injected in pharmacological doses, it is a vasodilator and antagonizes the pressor action of norepinephrine and angiotensin II; on the other hand, parathyroid hormone can potentiate the pressor effect of hypercalcemia.
本综述批判性地分析了有关钙、甲状旁腺激素和血压调节之间关系的现有信息。急性和慢性高钙血症均主要通过对血管平滑肌收缩性的直接作用来升高血压。通过激活激素升压系统产生间接作用的证据尚无定论。与高钙血症可导致高血压这一观点明显相反的是,最近有人提出钙缺乏在人类和自发性高血压动物的高血压发生过程中可能起重要作用。然而,支持这一观点的证据仍然相互矛盾。甲状旁腺激素对心血管系统发挥复杂的作用。一方面,如果以药理剂量注射,它是一种血管舒张剂,可拮抗去甲肾上腺素和血管紧张素II的升压作用;另一方面,甲状旁腺激素可增强高钙血症的升压作用。