Levy M
Department of Physiology, McGill University, Montreal, Quebec, Canada.
Semin Nephrol. 1997 Nov;17(6):520-9.
Atrial natriuretic peptide is one of a family of natriuretic peptides thought to play a role in the altered sodium balance of advanced liver disease and ascites. Its level is usually increased in the plasma of cirrhotic patients, probably due to relative plasma volume expansion. When exogenous ANP is administered intravenously to dogs or rats with experimental liver cirrhosis and ascites, an heterogeneous natriuretic response is obtained with about half of the population not responding. Similar observations are recorded for patients with clinical cirrhosis. In dogs, attenuation of the ANP-induced natriuresis may depend on a reduction in renal cortical bradykinin activity. In patients with cirrhosis, the ability to release ANP in response to central volume expansion is dissociated from the accompanying natriuresis. Attenuation of the renal tubular response to ANP in this setting may be correlated to the degree of intrahepatic sinusoidal hypertension and associated augmented reflex sympathetic nervous activity to the kidneys. Actual tubular resistance to ANP may be due to reduced Na+ delivery to the inner medullary collecting duct and/or increased degradation of cyclic guanosine monophosphate.
心房利钠肽是利钠肽家族的一员，被认为在晚期肝病和腹水患者钠平衡改变中发挥作用。肝硬化患者血浆中其水平通常升高，可能是由于相对血浆容量扩张所致。当对患有实验性肝硬化和腹水的犬或大鼠静脉注射外源性心房利钠肽时，会得到异质性的利钠反应，约一半个体无反应。临床肝硬化患者也有类似观察结果。在犬中，心房利钠肽诱导的利钠作用减弱可能取决于肾皮质缓激肽活性降低。在肝硬化患者中，对中心容量扩张释放心房利钠肽的能力与伴随的利钠作用相分离。在此情况下，肾小管对心房利钠肽反应的减弱可能与肝内窦状隙高血压程度及相关的肾脏反射性交感神经活动增强有关。肾小管对心房利钠肽的实际抵抗可能是由于到达髓质内集合管的钠离子输送减少和/或环磷酸鸟苷降解增加所致。
