Kramer H J
Postgrad Med J. 1975 Aug;51(598):532-40. doi: 10.1136/pgmj.51.598.532.
Besides intrarenal physical factors and aldosterone, a natriuretic hormone has been postulated to modulate renal tubular sodium resorption in order to maintain body fluid homeostasis. To investigate the possible role of a natriuretic activity in sodium retention of chronic liver disease, the effects of plasma and plasma fraction IV from patients with cirrhosis of the liver and ascites on sodium transport of the isolated frog skin and on renal sodium excretion in the rat were compared to the antinatriferic and natriuretic effects of plasma from healthy subjects. While plasma from healthy individuals obtained following acute expansion of the extracellular fluid volume (ECV) significantly inhibited potential difference (PD) by -43·8 ± 5·5% and short circuit current (SCC) by -41·3 ± 1·7% when applied to the inner skin surface, control plasma and plasma from patients with liver cirrhosis and ascites affected PD by -3·8 ± 4·7% and -5·2 ± 3·7% and SCC by -7·3 ± 4·6% and -11·7 ± 2·5% respectively. Similar effects on PD and SCC were observed with plasma fractions IV. In contrast to fraction IV from ECV-expanded individuals, which caused marked diuresis and natriuresis when injected in the rat, fraction IV of plasma from cirrhotic patients failed to affect urinary flow rate, free-water clearance or renal sodium excretion. The results suggest that at least some patients with cirrhosis of the liver and sodium retention may lack an adequate humoral natriuretic activity sufficiently to promote renal sodium excretion.
除了肾内物理因素和醛固酮外，人们推测有一种利钠激素可调节肾小管对钠的重吸收，以维持体液平衡。为了研究利钠活性在慢性肝病钠潴留中的可能作用，将肝硬化腹水患者的血浆和血浆组分IV对离体蛙皮钠转运及大鼠肾钠排泄的影响，与健康受试者血浆的抗利钠和利钠作用进行了比较。当将细胞外液量（ECV）急性扩张后获得的健康个体血浆应用于蛙皮内表面时，可使电位差（PD）显著降低-43·8±5·5%，短路电流（SCC）显著降低-41·3±1·7%；而对照血浆以及肝硬化腹水患者的血浆分别使PD降低-3·8±4·7%和-5·2±3·7%，使SCC降低-7·3±4·6%和-11·7±2·5%。血浆组分IV对PD和SCC也有类似影响。与ECV扩张个体的组分IV不同，后者注入大鼠后可引起明显的利尿和利钠作用，而肝硬化患者血浆的组分IV未能影响尿流率、自由水清除率或肾钠排泄。结果表明，至少部分肝硬化并伴有钠潴留的患者可能缺乏足够的体液利钠活性来促进肾钠排泄。
