心房利钠肽、C型利钠肽和一氧化氮在大鼠视网膜中诱导的环3',5'-鸟苷单磷酸合成

Cyclic 3',5'-guanosine monophosphate synthesis induced by atrial natriuretic peptide, C-type natriuretic peptide, and nitric oxide in the rat retina.

作者信息

Moriwaki Y, Kamisaki Y, Itoh T, Nagata M, Tamai A

机构信息

Department of Ophthalmology, Faculty of Medicine, Tottori University, Yonago, Japan.

出版信息

Jpn J Ophthalmol. 1998 Jul-Aug;42(4):269-74. doi: 10.1016/s0021-5155(98)00009-4.

DOI:10.1016/s0021-5155(98)00009-4

PMID:9749866

Abstract

This study was undertaken to determine whether pathways exist in the rat retina for atrial natriuretic peptide (ANP)-, C-type natriuretic peptide (CNP)-, and nitric oxide (NO)- cyclic 3', 5'-guanosine monophosphate (cGMP). Exposure of the retina to ANP (10(-7) mol/L), CNP (10(-7) mol/L), S-nitroso-N-acetylpenicillamine (10(-5) mol/L, SNAP; a NO donor), A23187 (10(-5)mol/L; a Ca2+ ionophore), and carbachol (10(-3) mol/L) caused 1.45 approximately 1.67-fold increases in cGMP content (P < .01). The increase in cGMP content induced by A23187 was blocked by 2-4-carboxyphenyl . 4455-tetramethyl imidazoline 1-oxyl 3-oxide (10(-3) mol/ L, carboxy-PTIO; a NO scavenger). Both carboxy-PTIO (10(-3) mol/L) and NG-nitro-L-arginine (10(-3) mol/L, L-NNA: a NO synthase inhibitor) blocked the increase in cGMP content induced by carbachol. Atropine (10(-50 mol/L; a muscarinic receptor antagonist) also blocked the cGMP increase induced by carbachol. These data demonstrate that ANP-, CNP-, and NO-cGMP pathways exist in the rat retina and that the NO-cGMP pathway may be linked to the activation of the muscarinic receptor.

摘要

本研究旨在确定大鼠视网膜中是否存在心房利钠肽（ANP）、C型利钠肽（CNP）和一氧化氮（NO）-环磷酸鸟苷（cGMP）的信号通路。将视网膜暴露于ANP（10⁻⁷mol/L）、CNP（10⁻⁷mol/L）、S-亚硝基-N-乙酰青霉胺（10⁻⁵mol/L，SNAP；一种NO供体）、A23187（10⁻⁵mol/L；一种Ca²⁺离子载体）和卡巴胆碱（10⁻³mol/L）可使cGMP含量增加1.45至1.67倍（P <.01）。A23187诱导的cGMP含量增加被2-（4-羧基苯基）-4,4,5,5-四甲基咪唑啉-1-氧化物（10⁻³mol/L，羧基-PTIO；一种NO清除剂）阻断。羧基-PTIO（10⁻³mol/L）和NG-硝基-L-精氨酸（10⁻³mol/L，L-NNA：一种NO合酶抑制剂）均可阻断卡巴胆碱诱导的cGMP含量增加。阿托品（10⁻⁵mol/L；一种毒蕈碱受体拮抗剂）也可阻断卡巴胆碱诱导的cGMP增加。这些数据表明，大鼠视网膜中存在ANP-、CNP-和NO-cGMP信号通路，且NO-cGMP信号通路可能与毒蕈碱受体的激活有关。