Kazda S, Grunt M, Hirth C, Preis W, Stasch J P
Institute of Pharmacology, Bayer AG, Wuppertal, Federal Republic of Germany.
J Hypertens Suppl. 1987 Dec;5(4):S37-42. doi: 10.1097/00004872-198712004-00007.
Calcium antagonism of nifedipine, nitrendipine or nisoldipine prevented salt-induced hypertension, renovascular damage and mortality in Dahl salt-sensitive (S) rats. The calcium agonist BAY K 8644 accelerated the development of salt-induced hypertension in S rats. In some S rats on a low-salt diet BAY K 8644 induced renovascular damage without sustained hypertension. In stroke-prone spontaneously hypertensive rats (SHRSP) on a normal diet the natural appearance of stroke was correlated with an increased calcium content in brain and kidney tissue. Nimodipine prevented stroke and the increase in brain calcium content without affecting the high blood pressure. A similar protective effect without substantial influence on high blood pressure was achieved by bilateral parathyroidectomy. Hypertension-associated vascular damage does not necessarily depend on the systemic intravascular pressure. In malignant hypertension the deleterious calcium overload in tissues may be activated or inhibited independently of the regulation of arterial blood pressure.
硝苯地平、尼群地平或尼索地平的钙拮抗作用可预防Dahl盐敏感（S）大鼠的盐诱导性高血压、肾血管损伤和死亡。钙激动剂BAY K 8644加速了S大鼠盐诱导性高血压的发展。在一些低盐饮食的S大鼠中，BAY K 8644在无持续性高血压的情况下诱发了肾血管损伤。在正常饮食的易中风自发性高血压大鼠（SHRSP）中，中风的自然发生与脑和肾组织中钙含量的增加相关。尼莫地平可预防中风和脑钙含量的增加，而不影响高血压。双侧甲状旁腺切除术也取得了类似的保护作用，且对高血压没有实质性影响。高血压相关的血管损伤不一定取决于全身血管内压力。在恶性高血压中，组织中有害的钙超载可能独立于动脉血压调节而被激活或抑制。
