Bruschi G, Regolisti G, Borghetti A
Istituto di Clinica Medica e Nefrologia, Università degli Studi di Parma.
Ann Ital Med Int. 1992 Jul-Sep;7(3 Suppl):119S-123S.
The control of vasomotion is a central issue in blood pressure regulation and is a primary goal of antihypertensive therapy. Calcium is the final messenger in the contractile mechanism of vascular smooth and cardiac muscle. Vasoconstrictor agents enhance the entry of Ca++ into vascular myocytes; vasodilators usually depress it. The most recent findings, based on direct measures of intracellular Ca++, have also highlighted the importance of calcium-sensitization mechanisms: vasoconstrictors sensitize the contractile apparatus to Ca++; vasodilators have an opposite effect. Cell calcium control alterations have been reported in different forms of hypertension. An increase in vascular myoplasmic Ca++ and a higher rate of calcium influx through specific, dihydropiridine-sensitive calcium channels have been found in genetic or secondary animal models. In hypertensive patients, an elevation of cytoplasmic Ca++ was noted in the platelets. Since Ca++ is a ubiquitous intracellular messenger, these changes may have profound implications for the pathophysiology of hypertension.
血管运动的控制是血压调节的核心问题，也是抗高血压治疗的主要目标。钙是血管平滑肌和心肌收缩机制中的最终信使。血管收缩剂可增强Ca++进入血管肌细胞；血管扩张剂通常会抑制这种进入。基于对细胞内Ca++的直接测量的最新研究结果也突出了钙敏化机制的重要性：血管收缩剂使收缩装置对Ca++敏感；血管扩张剂则有相反的作用。在不同类型的高血压中都有细胞钙控制改变的报道。在遗传性或继发性动物模型中发现血管肌浆Ca++增加以及通过特定的、对二氢吡啶敏感的钙通道的钙内流速率更高。在高血压患者中，血小板中的细胞质Ca++升高。由于Ca++是一种普遍存在的细胞内信使，这些变化可能对高血压的病理生理学产生深远影响。
