Plasma
renin activity (PRA), plasma
renin concentration (PRC),
angiotensinogen,
angiotensin II (AT II) and plasma
aldosterone were determined by radioimmunoassay in 77 patients with
cirrhosis of the liver [group I: with
ascites, untreated (n=23); group II: patients with
ascites during treatment (n=32); group III: after removal of fluids, but under further
spironolactone therapy (n=10); group IV: untreated subjects without
ascites (n=12)]. With the exception of decreased
angiotensinogen values in all groups ranging between 39% (group IV) and 73% (group III) no significant changes of the other parameters of the RAAS were found in untreated patients. A highly significant increase of PRA, PRC, AT II and plasma
aldosterone was observed in treated cirrhotics with (group II) or without (group III)
ascites. In the total series of patients AT II was closely related to PRA, PRC and
aldosterone emphasizing
aldosterone secretion. Plasma
sodium was inversely correlated to PRA, PRC, AT II and
aldosterone, but no relationship was detected between these parameters of the RAAS and plasma
potassium. Our results indicate that
hyperaldosteronism in
cirrhosis appears unlikely to be the major determinant of avid renal
sodium retention and
ascites formation. An increased activity of the RAAS is most often initiated by therapeutic factors and/or markedly altered
electrolyte metabolism. Therefore, basal conditions of the patients to be studied must be well defined to exclude any artificially induced stimulation of the RAAS.