title: Renin-angiotensin system in sepsis.
abstract: The time course of the components of the renin-angiotensin system was investigated in the plasma of three patients on the intensive care unit. Two of them, which were both polytraumatized, suffered from adult respiratory distress syndrome (ARDS). All patients had sepsis and impaired pulmonary and renal function. Plasma samples were investigated for up to two weeks, in which time all three patients showed a decrease in their angiotensin converting enzyme (ACE) plasma concentration. Two of the patients with deteriorating renal function had three to four times elevated angiotensinogen (Ao) plasma levels, which were measured by both the direct and indirect radioimmunoassay. The ratio of the mean values between both assays was 1:1 in two patients and shifted to higher values in the direct assay in the third patient. This suggests that higher amounts of des-AngI-angiotensinogen were present in the latter patient, because "inactive" Ao is also detected by the direct assay. The decrease in active Ao may be caused by an up to twenty times elevated plasma renin activity (PRA). The PRA was correlated with the angiotensin I (AngI) plasma levels. However, at PRA values higher than 200 pmol AngI/ml/h this correlation decreased because of the rapid substrate consumption. In addition there was a good correlation between AngI and AngII plasma levels in two patients which could not be observed in the patient with the highest PRA and AngII values. A relationship between plasma ACE concentration and AngII formation could not be observed. Thus in two of the three septic patients the components of the renin angiotensin system were extremely stimulated at very low blood pressure values. These data show, that it is reasonable to follow the time course of the components of the renin angiotensin system in single patients. In addition it is demonstrated that the direct measurement of Ao is a valid supplement in the diagnosis of the renin angiotensin system.
authors.affiliation: Pharmakologisches Institut, Universität Heidelberg, Fed. Rep. Germany.
authors.forename: U
authors.initials: U
authors.lastname: Hilgenfeldt
authors.forename: G
authors.initials: G
authors.lastname: Kienapfel
authors.forename: W
authors.initials: W
authors.lastname: Kellermann
authors.forename: R
authors.initials: R
authors.lastname: Schott
authors.forename: M
authors.initials: M
authors.lastname: Schmidt
mesh_terms: D058186:Acute Kidney Injury / Q000097:blood / Q000188:drug therapy / Q000209:etiology; D000803:Angiotensin I / Q000097:blood; D000804:Angiotensin II / Q000097:blood; D004837:Epinephrine / Q000494:pharmacology / Q000627:therapeutic use; D005665:Furosemide / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D009104:Multiple Trauma / Q000150:complications; D007703:Peptidyl-Dipeptidase A / Q000097:blood; D011014:Pneumonia / Q000150:complications; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000187:drug effects; D012128:Respiratory Distress Syndrome / Q000209:etiology / Q000503:physiopathology; D018805:Sepsis / Q000097:blood / Q000209:etiology / Q000503:physiopathology*
chemical_list: D000804:Angiotensin II; D005665:Furosemide; D000803:Angiotensin I; D007703:Peptidyl-Dipeptidase A; D012083:Renin; D004837:Epinephrine