Agnoli G C, Borgatti R, Cacciari M, Garutti C, Ikonomu E, Lenzi P, Marinelli M
Cattedra di Semeiotica Medica, Istituto di Clinica Medica II dell'Università di Bologna, Italy.
Clin Physiol. 1990 Jul;10(4):345-62. doi: 10.1111/j.1475-097x.1990.tb00796.x.
During hypotonic polyuria renal function studies by the clearance (cl.) method, and urinary PGE2, 6-keto-PGF1 alpha and TxB2 determinations were performed on 14 healthy women in normal potassium balance (N) and 14 healthy women in sustained potassium depletion (KD) induced by low dietary potassium intake (less than or equal to 10 mmol day-1) and natriuretic treatment. By using different depletive patterns, two groups with estimated cumulative potassium deficits of 160 +/- 43 mmol (KD1, n = 8) and 198 +/- 22 mmol (KD2, n = 6), respectively, were obtained. (1) In both the KD1 and KD2 groups as compared to normal potassium balance (N), plasma potassium concentration and urinary potassium excretion were significantly lower; plasma renin activity was significantly higher. (2) Only in KD2 did significant changes appear in renal function and urinary prostanoid excretions. Besides a decrease in creatinine cl. and the urinary flow rate, an increase in fractional chloride excretion and a reduction in distal fractional chloride reabsorption were manifest. The plasma chloride concentration was reduced too. Urinary prostanoid excretions were significantly (6-keto-PGF1 alpha, TxB2) or tendentially (PGE2) lower. (3) Indomethacin treatment resulted in changes in mean arterial pressure (increase) and creatinine cl. (decrease) which were not significantly different in normal potassium balance and KD groups. Only in KD2 did the drug significantly reduce the fractional salt and water excretions and the fractional sodium and chloride deliveries to the diluting segments. However, indomethacin was unable to correct the inhibition of distal fractional chloride reabsorption. Therefore, the potassium depletion attained in the KD2 group was efficacious in depressing renal prostanoid synthesis. This fact, in the presence of high levels of angiotensin II, induced a reduction of the glomerular filtration rate thus contributing to renal ability to retain chloride and potassium.
在通过清除率(cl.)方法进行的低渗性多尿肾功能研究中,对14名钾平衡正常(N)的健康女性和14名因低膳食钾摄入量(≤10 mmol/天)和利钠治疗导致持续性钾缺乏(KD)的健康女性进行了尿PGE2、6-酮-PGF1α和TxB2测定。通过采用不同的耗竭模式,分别获得了两组估计累积钾缺乏量为160±43 mmol(KD1,n = 8)和198±22 mmol(KD2,n = 6)的患者。(1)与正常钾平衡(N)组相比,KD1和KD2组的血浆钾浓度和尿钾排泄均显著降低;血浆肾素活性显著升高。(2)仅在KD2组中,肾功能和尿类前列腺素排泄出现了显著变化。除了肌酐清除率和尿流率降低外,氯排泄分数增加,远端氯重吸收分数降低也很明显。血浆氯浓度也降低了。尿类前列腺素排泄显著降低(6-酮-PGF1α、TxB2)或呈下降趋势(PGE2)。(3)吲哚美辛治疗导致平均动脉压(升高)和肌酐清除率(降低)发生变化,在正常钾平衡组和KD组中差异不显著。仅在KD2组中,该药物显著降低了盐和水的排泄分数以及输送到稀释段的钠和氯分数。然而,吲哚美辛无法纠正远端氯重吸收的抑制。因此,KD2组达到的钾缺乏有效地抑制了肾类前列腺素的合成。在血管紧张素II水平较高的情况下,这一事实导致肾小球滤过率降低,从而有助于肾脏保留氯和钾的能力。