Mujais S K
Department of Medicine, Northwestern University Medical School, Chicago, Illinois 60611.
Am J Physiol. 1994 Mar;266(3 Pt 2):F419-24. doi: 10.1152/ajprenal.1994.266.3.F419.
Potassium depletion is associated with a hyperreninemia that may be responsible for some of the renal hemodynamic and functional changes observed in K-deficient states. The present study was designed to evaluate whether interruption of the renin-angiotensin system with enalapril alters the collecting duct changes observed in K depletion. Adrenalectomized male Sprague-Dawley rats were allocated to either a normal (NK) or low-K diet (LK), and they either received enalapril or vehicle for 3 wk. Na:K pump activity (pmol.mm-1.h-1) in microdissected cortical collecting (CCT) and medullary collecting tubules (MCT) was determined at 21 days after group allocations. K depletion had a minimal effect on CCT outer diameter. In contrast, a marked hypertrophy was observed in the MCT diameter (91% increase, P < 0.001) that was significantly attenuated by enalapril treatment (56% increase, P < 0.001 vs. LK). An increase in Na:K pump activity was observed with LK, in the CCT from 497 +/- 47 to 1,089 +/- 83 (P < 0.001) and in the MCT from 489 +/- 36 to 1,396 +/- 45 pmol.mm-1.h-1 (P < 0.01). In K-replete rats, enalapril had no effect on Na:K pump activity in either CCT or MCT. Enalapril administration during LK had no effect on the increase in Na:K pump activity in the CCT (1,023 +/- 75 pmol.mm-1.h-1, P < 0.001), not different from LK alone. In the MCT, however, enalapril reduced the increment in Na:K pump activity induced by LK (1,116 +/- 39 pmol.mm-1.h-1, less than the change with LK alone).(ABSTRACT TRUNCATED AT 250 WORDS)
钾缺乏与高肾素血症有关,高肾素血症可能是钾缺乏状态下观察到的一些肾脏血流动力学和功能变化的原因。本研究旨在评估用依那普利阻断肾素-血管紧张素系统是否会改变钾缺乏时观察到的集合管变化。将肾上腺切除的雄性Sprague-Dawley大鼠分为正常(NK)或低钾饮食(LK)组,它们接受依那普利或赋形剂治疗3周。在分组21天后,测定显微解剖的皮质集合管(CCT)和髓质集合管(MCT)中的钠钾泵活性(pmol·mm⁻¹·h⁻¹)。钾缺乏对CCT外径影响最小。相比之下,观察到MCT直径显著增大(增加91%,P<0.001),依那普利治疗可使其显著减轻(增加56%,与LK组相比P<0.001)。LK组观察到钠钾泵活性增加,CCT中从497±47增加到1089±83(P<0.001),MCT中从489±36增加到1396±45 pmol·mm⁻¹·h⁻¹(P<0.01)。在钾充足的大鼠中,依那普利对CCT或MCT中的钠钾泵活性均无影响。LK期间给予依那普利对CCT中钠钾泵活性的增加无影响(1023±75 pmol·mm⁻¹·h⁻¹,P<0.001),与单独LK组无差异。然而,在MCT中,依那普利减少了LK诱导的钠钾泵活性增加(1116±39 pmol·mm⁻¹·h⁻¹,小于单独LK组的变化)。(摘要截断于250字)