VIP RECEPTOR-EFFECTOR SYSTEM IN LIVER MEMBRANES FROM CHOLESTATIC RATS

被引：5

作者：

RODRIGUEZHENCHE, N ^{[1
]}

GUIJARRO, LG ^{[1
]}

BAJO, AM ^{[1
]}

ARILLA, E ^{[1
]}

PRIETO, JC ^{[1
]}

机构：

[1] UNIV ALCALA DE HENARES, DEPT BIOQUIM & BIOL MOLEC, UNIDAD NEUROENDOCRINOL MOLEC, E-28871 ALCALA DE HENARES, SPAIN

来源：

PEPTIDES | 1994年 / 15卷 / 02期

关键词：

VASOACTIVE INTESTINAL PEPTIDE (VIP); GLUCAGON; VIP BINDING SITES; G(S)-PROTEIN; BILE DUCT LIGATION; ADENYLYL CYCLASE;

D O I：

10.1016/0196-9781(94)90023-X

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

A reduced efficacy of VIP (43% of the control) without modification in its potency (ED50 = 2.2 nM) was observed in regenerating rat liver after cholestasis (bile duct ligation). The same occurred with glucagon-stimulated adenylyl cyclase activity because the efficacy of this VIP-related peptide was also reduced (53% of the control) without changes in its potency in this experimental model. The equilibrium binding data revealed no changes in either the affinity or the VIP binding capacity of liver membranes during cholestasis. Cross-linking experiments gave the same apparent molecular mass for the liver VIP-receptor complex (52 kDa) in control and cholestatic rats. The coupling between the VIP receptor and the G(s)-protein was also unaffected because the sensitivity of VIP binding to GTP did not change after bile duct ligation. However, liver membranes from cholestatic rats showed a low extent of both ADP-ribosylation of the G(s)-protein alpha subunit (as assessed with cholera toxin) and adenylyl cyclase stimulation by a direct effector such as forskolin. Thus, VIP-stimulated adenylyl cyclase activity is decreased in regenerating liver after cholestasis due probably to an impairment in the interaction between G(s)-protein and adenylyl cyclase as well as a defect in the enzyme itself.

引用

页码：353 / 357

页数：5

共 44 条

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