Budzik G P, Firestone S L, Bush E N, Connolly P J, Rockway T W, Sarin V K, Holleman W H
Biochem Biophys Res Commun. 1987 Apr 14;144(1):422-31. doi: 10.1016/s0006-291x(87)80527-2.
ANF analog potencies in stimulating smooth muscle cell cGMP were compared with the ability to relax histamine-constricted rabbit aorta in vitro. ANF[1-28], [5-28], [5-27] and Lys-11[5-28] elevated cGMP and were potent vasorelaxants. ANF[7-23] and Lys-11[7-23] were potent cGMP stimulators but 1000-fold weaker relaxants. Tyr-8[5-27] did not stimulate cGMP synthesis or antagonize the response of the other peptides, yet was a potent vasorelaxant. Crosslinking with 125I-ANF identified bands at 150 and 65 KD by SDS-PAGE. ANF[1-28], Lys-11[7-23] and Tyr-8[5-27] blocked crosslinking at low concentration despite disparate activities. These data support the existence of ANF receptor subtypes and suggest that cGMP elevation alone is not sufficient to promote atrial peptide-induced vasorelaxation.
将心房钠尿肽（ANF）类似物刺激平滑肌细胞中环鸟苷酸（cGMP）的能力与它们在体外舒张组胺收缩的兔主动脉的能力进行了比较。ANF[1-28]、[5-28]、[5-27]和赖氨酸-11[5-28]可升高cGMP，并且是强效血管舒张剂。ANF[7-23]和赖氨酸-11[7-23]是强效的cGMP刺激剂，但作为血管舒张剂的作用弱1000倍。酪氨酸-8[5-27]不刺激cGMP合成，也不拮抗其他肽的反应，但却是一种强效血管舒张剂。用125I-ANF进行交联，通过十二烷基硫酸钠-聚丙烯酰胺凝胶电泳（SDS-PAGE）鉴定出150和65千道尔顿（KD）的条带。尽管活性不同，但ANF[1-28]、赖氨酸-11[7-23]和酪氨酸-8[5-27]在低浓度时可阻断交联。这些数据支持心房钠尿肽受体亚型的存在，并表明仅cGMP升高不足以促进心房肽诱导的血管舒张。
