Meyer P, Marche P
Department of Pharmacology, Hospital Necker, Paris, France.
Am J Med Sci. 1988 Apr;295(4):396-9. doi: 10.1097/00000441-198804000-00029.
Several alterations in membrane transport systems are observed in rat and human hypertension. Na+ flux changes are numerous, and cellular homeostasis to Na+ loading is impaired. Transmembrane Ca2+ movements are also numerous but clearly defined by a reduction in Ca2+ binders, a hypersensitivity of membrane phospholipase C, possible increased Ca2+ leak and reduced sensitivity of the Ca2+-pump to calmodulin. The resulting Ca2+ increase within arterial cells can be responsible for increased contractility and tone, leading to hypertension. These functional alterations in membrane transport can be secondary to a few well-defined membrane defects of genetic origin or to a diffuse structural perturbation in membranes involving lipid changes.
在大鼠和人类高血压中观察到膜转运系统的几种改变。钠通量变化众多，细胞对钠负荷的稳态受损。跨膜钙运动也很多，但明确表现为钙结合蛋白减少、膜磷脂酶C超敏、可能的钙泄漏增加以及钙泵对钙调蛋白的敏感性降低。动脉细胞内由此导致的钙增加可导致收缩性和张力增加，从而引发高血压。膜转运中的这些功能改变可能继发于一些明确的遗传起源的膜缺陷，或继发于涉及脂质变化的膜的弥漫性结构扰动。
