SYSTEMIC HYPOTENSION AND DIURESIS BY L-ARGININE IN CIRRHOTIC-PATIENTSWITH ASCITES - ROLE OF NITRIC-OXIDE

Citation
K. Tajiri et al., SYSTEMIC HYPOTENSION AND DIURESIS BY L-ARGININE IN CIRRHOTIC-PATIENTSWITH ASCITES - ROLE OF NITRIC-OXIDE, Hepatology, 22(5), 1995, pp. 1430-1435
Citations number
27
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
02709139
Volume
22
Issue
5
Year of publication
1995
Pages
1430 - 1435
Database
ISI
SICI code
0270-9139(1995)22:5<1430:SHADBL>2.0.ZU;2-9
Abstract
To investigate the role of nitric oxide in renal function and hemodyna mics in cirrhotic patients with ascites, L- arginine (30 g in 300 mL o f distilled water), a substrate for nitric oxide synthase, was infused into six cirrhotic patients with ascites, and the effects were compar ed with those of saline infusion. Healthy controls (n = 5) were also s tudied under the same conditions. In the patients, L-arginine infusion significantly decreased systolic and diastolic blood pressures while markedly increasing urinary flow and urinary sodium excretion; no sign ificant changes were seen with saline infusion. In controls, only dias tolic blood pressure was decreased by L-arginine infusion, whereas uri nary now and urinary sodium excretion were increased by both L-arginin e and saline infusion. In both groups, a similar increase of plasma at rial natriuretic factor (ANF) was seen with L-arginine and saline infu sions; endotheline and catecholamines were not affected by either infu sion. In both groups, plasma levels of vasopressin were increased by L -arginine infusion. In the cirrhotic patients, urinary excretions of c yclic guanosine monophosphate (cGMP) and nitrates/nitrites (NOx) were significantly increased by L-arginine infusion, whereas no significant changes were seen with saline infusion. In controls, only the excreti on of cGMP was increased by L-arginine infusion. In summary, L-arginin e infusion induces diuresis and natriuresis accompanied by increased e xcretions of cGMP and NOx in cirrhotic patients with ascites. This dif fers from the response in controls, where the increase in urinary sodi um excretion is not accompanied by an increase in markers of increased nitric oxide synthesis.