Gonzalez J M, Suki W N
Department of Medicine, Baylor College of Medicine, Houston, TX, USA.
Semin Nephrol. 1995 Nov;15(6):564-8.
In hypertensive humans and animals, intracellular calcium (Ca2+) has been found to be elevated in several cell types, including platelets, red blood cells, and smooth muscle cells. The messenger role of calcium requires its maintenance within cells at very low (submicromolar) ionic concentrations. This transcellular gradient is maintained by the reversible complexing of calcium to specific proteins. Intracellular free calcium can increase through an enhanced influx, release from intracellular stores, or a reduced efflux of calcium from the cell. Calcium channels are found to be increased in activity in some studies of hypertensive animals, but not in others. Sequestration of calcium within the cell has also been implicated in the increased cytosolic calcium in hypertension. Plasma membrane adenosine triphosphatases (ATPases) play a significant role in calcium extrusion; and the activity of these pumps has been found to be decreased in several human and animal studies. A single cause of the cellular calcium alterations in hypertension is not completely clear.
在高血压患者和动物中，已发现包括血小板、红细胞和平滑肌细胞在内的多种细胞类型的细胞内钙（Ca2+）升高。钙的信使作用要求其在细胞内维持非常低（亚微摩尔）的离子浓度。这种跨细胞梯度通过钙与特定蛋白质的可逆络合来维持。细胞内游离钙可通过增强的内流、从细胞内储存库释放或细胞内钙外流减少而增加。在一些高血压动物研究中发现钙通道活性增加，但在其他研究中未发现。细胞内钙的螯合也与高血压时细胞溶质钙增加有关。质膜三磷酸腺苷酶（ATPases）在钙的排出中起重要作用；在多项人体和动物研究中发现这些泵的活性降低。高血压时细胞钙改变的单一原因尚不完全清楚。
