We found a match
Your institution may have rights to this item. Sign in to continue.
- Title
Role of vasopressin in impaired water excretion in conscious rats with experimental cirrhosis.
- Authors
Linas, Stuart L.; Anderson, Robert J.; Guggenheim, Stephen J.; Robertson, Gary L.; Berl, Tomas; Dickmann, David C.
- Abstract
The present study was undertaken to study the mechanism of impaired water excretion in experimental cirrhosis in the rat. Conscious rats in whom histologically proven cirrhosis was induced with carbon tetrachloride and phenobarbital were compared with control rats given phenobarbital alone. Impaired water excretion in experimental cirrhosis was verified by a basal hyponatremia (138 vs. 147 mEq/liter, P < 0.005) and an impaired excretion of water load (minimal urinary osmolality. 262 vs. 100 mOsm/kg; 58 vs. 102% of water load excreted. P < 0.001). To clarify the mechanism of this impaired water excretion, we measured glomerular filtration rate (GFR), renal blood flow (RBF), and vasopressin (VP) levels. In cirrhosis. GFR was normal but RBF was decreased (4.5 vs 6.8 ml/min/g. P < 0.011. VP levels were found to be higher in cirrhotic rats (1.61 vs. 0.71 pg/ml, P < 0.025). The significance of the impaired renal hemodynamics and the increase in VP was assessed by inducing cirrhosis in VP-free Brattleboro (diabetes insipidus; Dl) rats. Despite histologic, biochemical, and renal hemodynamic changes that were comparable to cirrhotic rats with an intact neurohypophysis, cirrhotic Dl rats had no impairment in water excretion. To determine the cause of increased VP in experimental cirrhosis, we determined blood volume and systemic hemodynamics. Although plasma volume was greater in experimental cirrhosis (4.3 vs. 3.0 ml/100 g. P < 0.05). cirrhotic rats had a significantly lower peripheral resistance (0.37 vs. 0.42 mm Hg/ml/min/kg. P < 0.05) and mean arterial pressure (104 vs. 120 mm Hg, P < 0.001) than did control rats. These results document that experimental cirrhosis in the rat is associated with impaired renal water excretion in association with both abnormal renal hemodynamics and increased VP levels. The impaired water excretion, however, is solely VP mediated. The nonosmolar stimulus for VP release may be due to abnormal systemic hemodynamics.
- Subjects
VASOPRESSIN; EXCRETION; EXCRETORY organs; CIRRHOSIS of the liver; WATER in the body; GLOMERULAR filtration rate; KIDNEY glomerulus
- Publication
Kidney International, 1981, Vol 20, Issue 2, p173
- ISSN
0085-2538
- Publication type
Article
- DOI
10.1038/ki.1981.119