Schnapp P, Cernák P
Bratisl Lek Listy. 1989 Jun;90(6):454-7.
Following a two-week placebo period, a group of 10 elderly men (63-76 yrs) received a 20 mg nifedipine tablet each. Twelve hours later nifedipine, as compared to placebo, significantly raised diuresis, urine sodium excretion, and tubular sodium rejection, but had no affect GFR and urine potassium excretion. A significant drop in mean arterial pressure was registered six hours following nifedipine administration. After twelve hours, however, the statistical significance of the antihypertensive effect was reduced tenfold despite persisting natriuresis. In 4 elderly women (61-77 yrs), PRA level after nifedipine tended to rise, no such trend was observed for aldosterone. Although the mechanism of the natriuretic effect of Ca2+ channel blockers is not yet fully understood, it seems that the increase in Na+ excretion might be due to inhibition of Na+ reabsorption in renal tubules. It appears though as if the changes in Na+ excretion did not contribute to the acute BP decrease.
经过两周的安慰剂期后，一组10名老年男性（63 - 76岁）每人服用一片20毫克的硝苯地平片。12小时后，与安慰剂相比，硝苯地平显著增加了利尿、尿钠排泄和肾小管钠排泄，但对肾小球滤过率和尿钾排泄没有影响。硝苯地平给药6小时后，平均动脉压显著下降。然而，12小时后，尽管利钠作用持续存在，但降压效果的统计学显著性降低了10倍。在4名老年女性（61 - 77岁）中，硝苯地平后的肾素活性水平有上升趋势，醛固酮未观察到这种趋势。尽管钙通道阻滞剂利钠作用的机制尚未完全明了，但似乎钠排泄的增加可能是由于肾小管中钠重吸收的抑制。不过，钠排泄的变化似乎并未促成急性血压下降。
