[Renal and extra-renal mechanisms of sodium and water retention in cirrhosis with ascites].
In this work we analyze the renal and systemic factors involved in the sodium retention in two conditions: in extracellular volume depletion and in edema forming states, particularly liver cirrhosis with ascitis. In this paper we accept that the volume loss of body fluids stimulates the "effective arterial blood volume" (VAE). This term results from a decrease in the arterial blood volume secondary to a fall in cardiac output or a peripheral arterial vasodilatation. The reduction in the VAE stimulates: the high pressure baroreceptors (carotid sinus and aortic arch); the intrarrenal mechanisms, such as the yuxtaglomerular apparatus and the renin angiotensin aldosterone system; the sympathetic adrenergic system; the non osmotic release of antidiuretic hormone; prostaglandins (PGE1, Tromboxane) and endothelin; and inhibits the atrial natriuretic peptide. We also describe the sodium transport mechanisms along the nephron during physiological conditions and after volume depletion, and in edema formation states, specially hepatic cirrhosis with ascitis. We speculate that the intrarenal mechanisms are more important and persistent than the systemic mechanisms. It is possible that the sodium retention of these states might be the result of direct stimuli of the tubular sodium transport mechanisms in the different segments of the nephron, mediated by the co and counter transports, ATPase activity or by the second messengers cyclic AMP and cyclic GMP. The clonation and structural characterization of the different sodium transports may help us to establish, more precisely, the intracellular tubular mechanisms responsible for the tendency of the body to retain sodium. The amount of information generated in the future may help us to demonstrate, with more precision, the mechanisms responsible for the sodium retention and excretion in normal and pathological conditions, particularly the edema forming states such as cardiac failure, nephrotic syndrome and hepatic cirrhosis with ascitis.
Peña
J C
JC
Departamento de Nefrología y Metabolismo Mineral, Instituto Nacional de la Nutrición Salvador Zubirán, México, D.F.
D001201:Ascites; D001810:Blood Volume / Q000502:physiology; D001834:Body Water / Q000378:metabolism*; D002303:Cardiac Output, Low / Q000209:etiology / Q000503:physiopathology; D002319:Cardiovascular System / Q000503:physiopathology; D006728:Hormones / Q000502:physiology; D006801:Humans; D007668:Kidney / Q000503:physiopathology*; D008103:Liver Cirrhosis / Q000150:complications* / Q000503:physiopathology; D009569:Nitric Oxide / Q000502:physiology; D011311:Pressoreceptors / Q000502:physiology; D011453:Prostaglandins / Q000502:physiology; D012964:Sodium / Q000378:metabolism*; D013564:Sympathetic Nervous System / Q000503:physiopathology; D014883:Water-Electrolyte Imbalance / Q000209:etiology / Q000503:physiopathology*
D006728:Hormones; D011453:Prostaglandins; D009569:Nitric Oxide; D012964:Sodium
Mecanismos renales y extrarrenales en la retención de sodio y agua en la cirrosis con ascitis.