[Chronology of portal hypertension, decreased sodium excretion, and activation of the renin-angiotensin system in experimental biliary cirrhosis]. 1997

J L Poo, and A Estanes, and J Pedraza-Chaverrí, and C Cruz, and C Pérez, and A Huberman, and M Uribe
Departamentos de Gastroenterología, Instituto Nacional de la Nutrición, Salvador Zubirán, México, D.F.

OBJECTIVE 1) To evaluate the biochemical, renal, histological and splanchnic and systemic hemodynamic abnormalities induced by bile duct obstruction in rats, and 2) to study the temporal relationships between the start of portal hypertension, decrease of urinary sodium excretion and activation of the renin-angiotensin system. METHODS Bile duct obstruction was induced in 127 male Wistar rats, and renal function, hemodynamic, biochemical and liver histology were evaluated at weeks 1, 2, 3 and 4 after complete bile duct obstruction; the data were compared to that in 30 control rats. RESULTS Portal pressure significantly increased at week 1 (11.7 +/- 1.5. vs. 7.8 +/- 1.5 mmHg, p < 0.05) while the mean arterial pressure remained stable until week 4 when a slight decrease was observed (91.3 +/- 6.6 vs. 96.1 +/- 8.6 mmHg in control rats). A significant decrease in urinary sodium excretion was observed at week 1 (1.1 +/- 0.5 mEq/24 h) compared to control rats (2.3 +/- 0.6 mEq/24 h). In addition, hyperreninemia was observed at week 1 (5.1 +/- 0.2 vs. 2.4 +/- 1.3 ng Ang l/mL/h, p < 0.05) and hyperaldosteronism at week 2 (103 +/- 46 vs. 25.1 +/- 8.8 ng/24 h, p < 0.05) compared to control rats. CONCLUSIONS A temporal relationship between the beginning of portal hypertension and a decrease of renal sodium excretion, hyperreninemia and hyperaldosteronism was observed in bile duct ligated rats. This experimental model could be used to evaluate the effects of new drugs to prevent biliary cirrhosis including the abnormalities in the renal handling of sodium.

UI MeSH Term Description Entries
D006975 Hypertension, Portal Abnormal increase of resistance to blood flow within the hepatic PORTAL SYSTEM, frequently seen in LIVER CIRRHOSIS and conditions with obstruction of the PORTAL VEIN. Cruveilhier-Baumgarten Disease,Cruveilhier-Baumgarten Syndrome,Cruveilhier Baumgarten Disease,Cruveilhier Baumgarten Syndrome,Disease, Cruveilhier-Baumgarten,Portal Hypertension,Portal Hypertensions,Syndrome, Cruveilhier-Baumgarten
D007668 Kidney Body organ that filters blood for the secretion of URINE and that regulates ion concentrations. Kidneys
D008105 Liver Cirrhosis, Biliary FIBROSIS of the hepatic parenchyma due to obstruction of BILE flow (CHOLESTASIS) in the intrahepatic or extrahepatic bile ducts (BILE DUCTS, INTRAHEPATIC; BILE DUCTS, EXTRAHEPATIC). Primary biliary cholangitis involves the destruction of small intra-hepatic bile ducts and decreased bile secretion. Secondary biliary cholangitis is produced by prolonged obstruction of large intrahepatic or extrahepatic bile ducts from a variety of causes. Biliary Cirrhosis,Biliary Cirrhosis, Primary,Biliary Cirrhosis, Secondary,Cholangitis, Chronic Nonsuppurative Destructive,Liver Cirrhosis, Obstructive,Primary Biliary Cholangitis,Biliary Cirrhosis, Primary, 1,Primary Biliary Cirrhosis,Secondary Biliary Cholangitis,Secondary Biliary Cirrhosis,Biliary Cholangitides, Primary,Biliary Cholangitis, Primary,Biliary Cholangitis, Secondary,Cholangitides, Primary Biliary,Cholangitis, Primary Biliary,Cholangitis, Secondary Biliary,Cirrhosis, Biliary,Cirrhosis, Secondary Biliary,Liver Cirrhoses, Biliary,Obstructive Liver Cirrhosis,Primary Biliary Cholangitides,Secondary Biliary Cholangitides
D008297 Male Males
D012084 Renin-Angiotensin System A BLOOD PRESSURE regulating system of interacting components that include RENIN; ANGIOTENSINOGEN; ANGIOTENSIN CONVERTING ENZYME; ANGIOTENSIN I; ANGIOTENSIN II; and angiotensinase. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming ANGIOTENSIN I. Angiotensin-converting enzyme, contained in the lung, acts on angiotensin I in the plasma converting it to ANGIOTENSIN II, an extremely powerful vasoconstrictor. Angiotensin II causes contraction of the arteriolar and renal VASCULAR SMOOTH MUSCLE, leading to retention of salt and water in the KIDNEY and increased arterial blood pressure. In addition, angiotensin II stimulates the release of ALDOSTERONE from the ADRENAL CORTEX, which in turn also increases salt and water retention in the kidney. Angiotensin-converting enzyme also breaks down BRADYKININ, a powerful vasodilator and component of the KALLIKREIN-KININ SYSTEM. Renin-Angiotensin-Aldosterone System,Renin Angiotensin Aldosterone System,Renin Angiotensin System,System, Renin-Angiotensin,System, Renin-Angiotensin-Aldosterone
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D012964 Sodium A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23. Sodium Ion Level,Sodium-23,Ion Level, Sodium,Level, Sodium Ion,Sodium 23
D013997 Time Factors Elements of limited time intervals, contributing to particular results or situations. Time Series,Factor, Time,Time Factor
D017208 Rats, Wistar A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain. Wistar Rat,Rat, Wistar,Wistar Rats
D051381 Rats The common name for the genus Rattus. Rattus,Rats, Laboratory,Rats, Norway,Rattus norvegicus,Laboratory Rat,Laboratory Rats,Norway Rat,Norway Rats,Rat,Rat, Laboratory,Rat, Norway,norvegicus, Rattus

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