BACKGROUND: The renin-angiotensin system may be implicated in the subtle sodium handling abnormality in preascitic cirrhosis. AIMS: To assess the role of angiotensin II in sodium homoeostasis in preascitic cirrhosis, using losartan, its receptor antagonist. PATIENTS: Nine male, preascitic cirrhotic patients, and six age matched, healthy male controls. METHODS: A dose response study using 2.5, 5, 7.5, and 10 mg of losartan was performed on a daily 200 mmol sodium intake, followed by repeat studies with the optimal dose, 7.5 mg of losartan, to determine its effects on systemic and renal haemodynamics, renal sodium handling, and neurohumoral factors. RESULTS: Preascitic cirrhotic patients had significantly reduced baseline urinary sodium excretion compared with controls (154 (8) versus 191 (12) mmol/day, p<0.05), associated with significantly reduced systemic angiotensin II levels (6.0 (1.7) versus 39.5 (10.0) pmol/l, p=0.002). Losartan 7.5 mg normalised renal sodium handling in the preascitic cirrhotic patients (202 (12) mmol/day, p=0.05 versus baseline), without any change in systemic or renal haemodynamics, but with significantly increased systemic angiotensin II levels (7.8 (2.3) pmol/l, p=0.05 versus baseline). Losartan had no effect on renal sodium handling in controls. CONCLUSIONS: In preascitic cirrhotic patients, the subtle renal sodium retention, paradoxically associated with low systemic neurohumoral factor levels, is improved with low dose losartan, suggesting the involvement of angiotensin II via its direct action on the renal tubule.
BACKGROUND: The renin-angiotensin system may be implicated in the subtle sodiumhandling abnormality in preascitic cirrhosis. AIMS: To assess the role of angiotensin II in sodiumhomoeostasis in preascitic cirrhosis, using losartan, its receptor antagonist. PATIENTS: Nine male, preascitic cirrhoticpatients, and six age matched, healthy male controls. METHODS: A dose response study using 2.5, 5, 7.5, and 10 mg of losartan was performed on a daily 200 mmol sodium intake, followed by repeat studies with the optimal dose, 7.5 mg of losartan, to determine its effects on systemic and renal haemodynamics, renal sodium handling, and neurohumoral factors. RESULTS:Preascitic cirrhoticpatients had significantly reduced baseline urinary sodium excretion compared with controls (154 (8) versus 191 (12) mmol/day, p<0.05), associated with significantly reduced systemic angiotensin II levels (6.0 (1.7) versus 39.5 (10.0) pmol/l, p=0.002). Losartan 7.5 mg normalised renal sodium handling in the preascitic cirrhoticpatients (202 (12) mmol/day, p=0.05 versus baseline), without any change in systemic or renal haemodynamics, but with significantly increased systemic angiotensin II levels (7.8 (2.3) pmol/l, p=0.05 versus baseline). Losartan had no effect on renal sodium handling in controls. CONCLUSIONS: In preascitic cirrhoticpatients, the subtle renal sodium retention, paradoxically associated with low systemic neurohumoral factor levels, is improved with low dose losartan, suggesting the involvement of angiotensin II via its direct action on the renal tubule.
Authors: M Burnier; M Hagman; J Nussberger; J Biollaz; C Armagnac; R Brouard; B Weber; H R Brunner Journal: Hypertension Date: 1995-04 Impact factor: 10.190
Authors: M R Goldberg; T E Bradstreet; E J McWilliams; W K Tanaka; S Lipert; T D Bjornsson; S A Waldman; B Osborne; L Pivadori; G Lewis Journal: Hypertension Date: 1995-01 Impact factor: 10.190
Authors: I Crozier; H Ikram; N Awan; J Cleland; N Stephen; K Dickstein; M Frey; J Young; G Klinger; L Makris Journal: Circulation Date: 1995-02-01 Impact factor: 29.690
Authors: Regina Maria Pereira; Robson Augusto Souza dos Santos; Filipi Leles da Costa Dias; Mauro Martins Teixeira; Ana Cristina Simões e Silva Journal: World J Gastroenterol Date: 2009-06-07 Impact factor: 5.742