Merzon A K, Donskova T V, Zolotov N A, Kolomiets V V, Merzon K A
Ter Arkh. 1988;60(6):74-9.
Sublingual administration of nifedipine (N) at a dose of 20 mg to 8 persons without cardiovascular and renal pathology and to 19 patients with congestive heart failure (CHF) increased renal excretion of sodium (by an average of 51.1-132.8%), water (by an average of 31.7-101.9%), potassium (by an average of 43.2-63.2%) and calcium (by an average of 118%). The natriuretic effect of N appeared in 20 min reaching its maximum in 45-60 min, being more noticeable in CHF. An increment of natriuresis resulted from a decrease in sodium tubular reabsorption (correlation factor--0.92) rather than from an increase in glomerular filtration (correlation factor +0.50). N suppressed sodium reabsorption in the proximal tubule (by an average of 34.1%) as well as in the segment, more distal of Henle's loop (by an average of 6.8%). N might suppress directly calcium-dependent mechanisms of sodium transtubular transport but it could also produce a mediated effect as a result of shifts of renal hemodynamics.
对8名无心血管和肾脏病变的人和19名充血性心力衰竭(CHF)患者舌下含服20毫克硝苯地平(N),可增加钠(平均增加51.1 - 132.8%)、水(平均增加31.7 - 101.9%)、钾(平均增加43.2 - 63.2%)和钙(平均增加118%)的肾排泄。N的利钠作用在20分钟时出现,45 - 60分钟时达到最大,在CHF患者中更明显。利钠增加是由于肾小管对钠的重吸收减少(相关系数 - 0.92),而非肾小球滤过增加(相关系数 +0.50)。N抑制近端小管(平均34.1%)以及亨利氏袢更远端节段(平均6.8%)对钠的重吸收。N可能直接抑制钠跨肾小管转运的钙依赖机制,但也可能因肾血流动力学改变而产生介导作用。