López C, Jiménez W, Arroyo V, Gaya J, Rivera F, Rodés J
Laboratorio Hormonal y Unidad de Hepatología, Hospital Clínico Provincial, Universidad de Barcelona, Spain.
Rev Esp Fisiol. 1988 Sep;44(3):265-72.
Glomerular filtration rate, urine volume, sodium excretion and mean arterial pressure were measured in 10 rats with Cl4C induced cirrhosis presenting sodium retention and ascites, and in 10 control rats before and during the iv administration of the 28 aminoacid rat alpha-Atrial Natriuretic Peptide (alpha-ANP) (a bolus of 1 microgram followed by a constant infusion of 33 ng/min). alpha-ANP induced a similar increase in glomerular filtration rate and filtered sodium load in both groups of rats. In contrast, the increase in urine volume and sodium excretion produced by alpha-ANP was significantly lower in cirrhotic rats (from 13.8 +/- 1.9 to 37.9 +/- 9.1 microliters/min., and from 0.5 +/- 0.1 to 3.3 +/- 1.0 microEq/min) than in control animals (from 14.6 +/- 1.3 to 102.5 +/- 17.7 microliters/min., p less than 0.005; and from 1.0 +/- 0.3 to 14.1 +/- 3.2 microEq/min., p less than 0.001). The results indicate that in rats with experimental cirrhosis and ascites there are blunted diuretic and natriuretic responses to alpha-ANP, probably as a consequence of the exaggerated tubular sodium reabsorption present in these animals.
在10只由四氯化碳诱导产生肝硬化并伴有钠潴留和腹水的大鼠以及10只对照大鼠中,在静脉注射28个氨基酸的大鼠α-心房利钠肽(α-ANP)(先推注1微克,随后以33纳克/分钟的速度持续输注)之前和期间,测量了肾小球滤过率、尿量、钠排泄量和平均动脉压。α-ANP在两组大鼠中均引起肾小球滤过率和滤过钠负荷的相似增加。相比之下,α-ANP在肝硬化大鼠中产生的尿量和钠排泄量的增加(从13.8±1.9微升/分钟增加到37.9±9.1微升/分钟,以及从0.5±0.1微当量/分钟增加到3.3±1.0微当量/分钟)明显低于对照动物(从14.6±1.3微升/分钟增加到102.5±17.7微升/分钟,p<0.005;以及从1.0±0.3微当量/分钟增加到14.1±3.2微当量/分钟,p<0.001)。结果表明,在患有实验性肝硬化和腹水的大鼠中,对α-ANP的利尿和利钠反应减弱,这可能是这些动物肾小管钠重吸收过度的结果。