Romero J C, Raij L, Granger J P, Ruilope L M, Rodicio J L
Hypertension. 1987 Aug;10(2):140-51. doi: 10.1161/01.hyp.10.2.140.
Characterization of the renal effects of calcium entry blockers has not been easy because the inhibition of Ca2+ cellular influx alters several regulatory functions. The ability of calcium blockers to dilate renal vasculature and to increase glomerular filtration rate is largely determined by the preexisting vascular tone. However, the increments in sodium excretion could occur without alterations in renal hemodynamics. Calcium blockers could increase sodium excretion by inducing a redistribution of renal blood flow toward juxtamedullary nephrons, by inhibiting tubuloglomerular feedback responses, or by a direct action on the tubular transport of sodium. These effects are poorly understood at present. In vitro studies show that the blockade of calcium entry enhances renin secretion and decreases prostaglandin synthesis. This dissociation has not been found during long-term administration, which has been proved to be effective for the treatment of essential hypertension with normal maintenance of renal function. In this respect, there are reports indicating that calcium blockers are particularly effective in a subgroup of patients with essential hypertension who exhibit subtle but detectable alterations in calcium metabolism. Further studies are needed to determine whether this significant response to calcium blockers is due to correction of an early defect of calcium cellular kinetics that initiated the increase in blood pressure.
由于抑制Ca2+细胞内流会改变多种调节功能，因此对钙通道阻滞剂肾脏效应的表征并不容易。钙通道阻滞剂扩张肾血管和增加肾小球滤过率的能力很大程度上取决于预先存在的血管张力。然而，钠排泄增加可能在不改变肾脏血流动力学的情况下发生。钙通道阻滞剂可通过诱导肾血流向近髓肾单位重新分布、抑制肾小管-肾小球反馈反应或直接作用于肾小管钠转运来增加钠排泄。目前对这些作用了解甚少。体外研究表明，钙内流的阻断会增强肾素分泌并减少前列腺素合成。长期给药期间未发现这种分离现象，长期给药已被证明对治疗原发性高血压有效，且能维持正常肾功能。在这方面，有报告表明，钙通道阻滞剂在原发性高血压患者的一个亚组中特别有效，这些患者在钙代谢方面表现出细微但可检测到的改变。需要进一步研究以确定对钙通道阻滞剂的这种显著反应是否是由于纠正了引发血压升高的早期钙细胞动力学缺陷。
