摘要
Abstract Objective To investigate the changes of alpha 1 adrenergic receptors in cirrhotic liver and the relationship between the changes and the pathogenesis of portal hypertension. Methods The concentration and affinity of alpha 1 adrenergic receptors in the liver plasma membranes of posthepatitic cirrhotic patients with portal hypertension were quantitatively measured using radioligand binding analysis. Results Compared with 8 controls without hepatic pathological changes, the maximal binding capacity (Bmax) of 9 posthepatitic cirrhotic patients decreased (129.1±12.0 vs 142.1±14.1 fmol/mg protein, P>0.05), dissociation constant (Kd) values increased (0.3945±0.0974 vs 0.2382±0.0548 nmol/L, P< 0.01), and the receptor maximal content (RMC) decreased (417.4±76.8 vs 739.9±167.6 fmol/g liver, P<0.01). Conclusions The decreased concentration and affinity of alpha 1 adrenergic receptors may play an important role in the metabolic disturbances of catecholamines often seen in some cirrhotic patients, and have implications in the pathogenesis of portal hypertension.
Abstract Objective To investigate the changes of alpha 1 adrenergic receptors in cirrhotic liver and the relationship between the changes and the pathogenesis of portal hypertension. Methods The concentration and affinity of alpha 1 adrenergic receptors in the liver plasma membranes of posthepatitic cirrhotic patients with portal hypertension were quantitatively measured using radioligand binding analysis. Results Compared with 8 controls without hepatic pathological changes, the maximal binding capacity (Bmax) of 9 posthepatitic cirrhotic patients decreased (129.1±12.0 vs 142.1±14.1 fmol/mg protein, P>0.05), dissociation constant (Kd) values increased (0.3945±0.0974 vs 0.2382±0.0548 nmol/L, P< 0.01), and the receptor maximal content (RMC) decreased (417.4±76.8 vs 739.9±167.6 fmol/g liver, P<0.01). Conclusions The decreased concentration and affinity of alpha 1 adrenergic receptors may play an important role in the metabolic disturbances of catecholamines often seen in some cirrhotic patients, and have implications in the pathogenesis of portal hypertension.
