Smyth E M, Keenan A K
Department of Pharmacology, University College, Belfield, Dublin, Ireland.
Life Sci. 1994;54(1):1-7. doi: 10.1016/0024-3205(94)00571-0.
A role for the ANF-C receptor ligand des[Cys105,Cys121]rANF(104-126) in ANF receptor-effector coupling was investigated using cultured bovine pulmonary artery endothelial cells as a model system. The ligand was equipotent with rANF(99-126) in displacement of [125I]des[Cys105,Cys121]rANF(104-126) binding to whole cells and labelled only one population of ANF receptors as shown by affinity crosslinking experiments. In cells pretreated with des[Cys105, Cys121]rANF(104-126), internalization of [125I]rANF(99-126) binding was reduced and enhanced accumulation of cGMP was observed under basal conditions, or in the presence of a low concentration (0.1 nM) of rANF(99-126). These results provide a mechanistic basis for the observed enhancement of ANF-dependent vasodilation by ANF-C receptor selective ligands.
以培养的牛肺动脉内皮细胞作为模型系统，研究了心房钠尿肽-C受体配体des[Cys105，Cys121]rANF(104 - 126)在心房钠尿肽受体-效应器偶联中的作用。该配体在取代[125I]des[Cys105，Cys121]rANF(104 - 126)与全细胞结合方面与rANF(99 - 126)等效，并且如亲和交联实验所示，仅标记了一群心房钠尿肽受体。在用des[Cys105，Cys121]rANF(104 - 126)预处理的细胞中，[125I]rANF(99 - 126)结合的内化减少，并且在基础条件下或存在低浓度(0.1 nM)的rANF(99 - 126)时观察到环鸟苷酸的积累增加。这些结果为观察到的心房钠尿肽-C受体选择性配体增强心房钠尿肽依赖性血管舒张提供了机制基础。
