title: Urinary sodium retention in chronic liver disease: a summary.
abstract: In animal models of developing portal hypertension, sodium retention occurs for several reasons. Firstly, baroreceptors within the liver signal the renal tubule to retain sodium, irregardless of the extracellular fluid volume status or the status of systemic hemodynamics. Secondly, the requirements of the enlarging portal venous space also stimulate the renal tubule to retain sodium and expand plasma volume. During this period plasma levels of renin and aldosterone probably fall, and the circulation becomes overfilled. Eventually the Starling forces become quite disturbed. At this point, plasma levels of renin, aldosterone, catecholamines and antidiuretic hormone (ADH) begin to rise. Thus, the correct description of the appearance of ascites and the pathophysiology of sodium retention should reflect the biphasic nature of the magnitude of the plasma volume, which goes from a state of overfilling to one of underfilling.
mesh_terms: D000818:Animals; D001201:Ascites / Q000139:chemically induced; D003900:Desoxycorticosterone / Q000633:toxicity; D004285:Dogs; D006801:Humans; D006975:Hypertension, Portal / Q000139:chemically induced / Q000503:physiopathology*; D007273:Injections, Intramuscular; D008103:Liver Cirrhosis / Q000139:chemically induced / Q000503:physiopathology*; D010953:Plasma Volume; D012964:Sodium / Q000378:metabolism* / Q000633:toxicity
chemical_list: D003900:Desoxycorticosterone; D012964:Sodium