Abnormal sympathetic and renal response to sodium restriction in compensated cirrhosis.
It has been proposed that in liver cirrhosis portal hypertension causes splanchnic vasodilation and this induces blood volume expansion to maintain blood pressure. The current study was designed to explore the homeostatic response to sodium restriction, a maneuver aiming to contract blood volume, in compensated cirrhosis. Mean blood pressure, sympathetic nervous activity, and proximal sodium reabsorption were evaluated in 16 healthy control and 21 nonazotemic cirrhotic patients (11 without ascites and 10 with ascites) under two experimental conditions: after 4 days on a free sodium diet (basal condition) and after 4 days on a restricted sodium diet (40 mmol/day). No differences were observed in basal conditions in the above parameters between control and cirrhotic patients without ascites. However, cirrhotic patients with ascites showed lower basal values of mean blood pressure and higher basal levels of both plasma norepinephrine and fractional proximal sodium reabsorption than controls. Neither control nor cirrhotic patients with ascites showed significant changes in the measured parameters after sodium restriction. In contrast, in nonascitic patients, this maneuver induced an elevation in plasma norepinephrine concentration (164.4 +/- 24.6 vs. 270.1 +/- 24.9 pg/mL; mean +/- SEM; P less than 0.005) and in fractional proximal sodium reabsorption (86.4 +/- 2.1 vs. 91.8% +/- 0.5%; P less than 0.01). In addition, the nonascitic cirrhotic patients became hypotensive compared with controls (80.9 +/- 1.6 vs. 88.5 +/- 4.8 mm Hg; P less than 0.05) when subjected to the low-sodium diet. In patients without ascites, under conditions of sodium restriction, the decrease in mean arterial pressure correlated inversely with the increase in plasma norepinephrine concentration (r = -0.713; P less than 0.05), whereas the levels of plasma norepinephrine correlated directly with fractional proximal sodium reabsorption (r = 0.893; P less than 0.01). These findings suggest that ineffective circulatory volume is detected in nonascitic cirrhotic patients only under conditions of sodium restriction, but it is always present in cirrhotic patients with ascites, irrespectively of the amount of sodium in the diet. These results are compatible with the existence of fixed arterial vasodilation in cirrhosis.
Simón
M A
MA
Department of Medicine, Hospital Miguel Servet, Zaragoza, Spain.
Díez
J
J
Prieto
J
J
D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000097:blood; D001201:Ascites / Q000097:blood / Q000209:etiology / Q000503:physiopathology; D001794:Blood Pressure / Q000502:physiology; D001810:Blood Volume / Q000502:physiology*; D004039:Diet, Sodium-Restricted; D005260:Female; D006706:Homeostasis; D006801:Humans; D007684:Kidney Tubules / Q000503:physiopathology*; D008094:Lithium / Q000493:pharmacokinetics; D008103:Liver Cirrhosis / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D008297:Male; D008657:Metabolic Clearance Rate; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood; D012083:Renin / Q000097:blood; D012964:Sodium / Q000378:metabolism*; D014664:Vasodilation / Q000502:physiology
D000450:Aldosterone; D008094:Lithium; D012964:Sodium; D012083:Renin; D009638:Norepinephrine