Romero J C, Ruilope L M, Bentley M D, Fiksen-Olsen M J, Lahera V, Vidal M J
Department of Physiology and Biophysics, Mayo Clinic, Rochester, Minnesota 55905.
Am J Cardiol. 1988 Oct 5;62(11):59G-68G. doi: 10.1016/0002-9149(88)90034-3.
Calcium antagonists decrease the ability of the kidney to autoregulate renal blood flow (RBF) and glomerular filtration rate (GFR). Therefore, when afferent renovascular resistance is elevated, as in essential hypertension, there is a resultant increase in RBF and GFR with the administration of calcium antagonists. These agents also induce a marked natriuresis because of direct tubular action through unknown mechanisms. The natriuresis can be dissociated from renal and systemic hemodynamic actions, indicating that the decreased sodium reabsorption could override other compensatory mechanisms explaining the absence of sodium retention during the treatment. The renal effects of converting enzyme inhibitors (CEIs) can be explained by the reduction of intrarenal formation in angiotensin II. Because the activation of the renin-angiotensin system is mainly responsible for inducing sodium retention during a decrease in systemic blood pressure, CEIs could have a protecting effect without disturbing other homeostatic mechanisms. CEIs decrease efferent glomerular resistance, reducing capillary pressure and thereby reducing GFR. This effect is not translated in sodium retention because the reduction of GFR is mild during captopril administration in kidneys with normal or increased renal perfusion pressure. At low renal perfusion pressure, the reduced glomerular afferent vasoconstriction can compromise GFR, leading to renal insufficiency. Although these situations are not likely to be encountered during the treatment of uncomplicated essential hypertension, in severe hypertension with hypertrophy of pre-glomerular vessels, glomerular perfusion may decrease. Combination therapy of calcium antagonists and CEIs has been reported to be an effective treatment of severe hypertension. Currently, little information is available on the manner in which renal function is affected by simultaneous administration of both drugs.
钙拮抗剂会降低肾脏自身调节肾血流量（RBF）和肾小球滤过率（GFR）的能力。因此，当肾入球小动脉阻力升高时，如在原发性高血压中，使用钙拮抗剂会使RBF和GFR随之增加。这些药物还会通过未知机制直接作用于肾小管，从而引起显著的利钠作用。这种利钠作用可与肾脏和全身血流动力学作用相分离，这表明钠重吸收的减少可能会超越其他代偿机制，从而解释了治疗期间无钠潴留的原因。转换酶抑制剂（CEIs）的肾脏作用可以通过肾内血管紧张素II生成减少来解释。由于肾素-血管紧张素系统的激活是导致系统性血压下降时钠潴留的主要原因，CEIs可以在不干扰其他稳态机制的情况下发挥保护作用。CEIs可降低肾小球出球小动脉阻力，降低毛细血管压力，从而降低GFR。这种作用不会导致钠潴留，因为在肾灌注压力正常或升高的肾脏中，服用卡托普利期间GFR的降低程度较轻。在低肾灌注压力下，肾小球入球小动脉收缩减弱会损害GFR，导致肾功能不全。虽然在单纯原发性高血压的治疗过程中不太可能遇到这些情况，但在严重高血压且肾小球前血管肥厚的情况下，肾小球灌注可能会降低。据报道，钙拮抗剂与CEIs联合治疗是治疗严重高血压的有效方法。目前，关于同时服用这两种药物对肾功能影响方式的信息很少。
