Nitric oxide induces muscular relaxation via cyclic GMP-dependent and -independent mechanisms in the longitudinal muscle of the mouse duodenum

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Abstract

The aim of this study was to investigate, in mouse duodenum, the role of nitric oxide (NO) in the relaxation of longitudinal muscle evoked by nerve activation and the coupled action mechanism. Electrical field stimulation (EFS; 0.5ms, 10-s train duration, supramaximal voltage, at various frequencies) under nonadrenergic noncholinergic conditions evoked muscular relaxation occasionally followed, at the higher stimulus frequencies, by rebound contractions. Inhibition of the synthesis of NO by Nω-nitro-L-arginine methyl ester (L-NAME; 100μM) virtually abolished the evoked relaxation. The relaxation was reduced also by apamin (0.1μM) and by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 1μM), a guanylyl cyclase inhibitor. The coadministration of apamin and ODQ produced additive effects on the responses to EFS. Sodium nitroprusside (0.1-100μM) produced a concentration-dependent reduction of the phasic spontaneous activity and at the highest dose used suppressed phasic activity and induced muscular relaxation. These effects were tetrodotoxin and L-NAME resistant and were antagonized both by apamin and by ODQ. 8-Bromoguanosine 3′,5′-cyclic monophosphate (0.1-100μM) reduced in a concentration-dependent manner the spontaneous mechanical activity and at 100μM suppressed the phasic activity and induced muscular relaxation, not antagonized by apamin. This study indicates that NO is the primary transmitter released by inhibitory nerves supplying the longitudinal muscle of mouse duodenum and that guanylate cyclase stimulation and opening of Ca2+-dependent K+ channels are independent mechanisms working in parallel to mediate NO action. © 2002 Elsevier Science (USA). All rights reserved.
Lingua originaleEnglish
pagine (da-a)48-52
Numero di pagine5
RivistaNITRIC OXIDE
Volume8
Stato di pubblicazionePublished - 2003

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Apamin
Cyclic GMP
Duodenum
Muscle
Nitric Oxide
Muscles
Guanylate Cyclase
NG-Nitroarginine Methyl Ester
Arginine
Muscle Relaxation
Tetrodotoxin
Nitroprusside
Electric Stimulation
Transmitters
Esters
Chemical activation
Electric potential

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Physiology
  • Clinical Biochemistry
  • Cancer Research

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title = "Nitric oxide induces muscular relaxation via cyclic GMP-dependent and -independent mechanisms in the longitudinal muscle of the mouse duodenum",
abstract = "The aim of this study was to investigate, in mouse duodenum, the role of nitric oxide (NO) in the relaxation of longitudinal muscle evoked by nerve activation and the coupled action mechanism. Electrical field stimulation (EFS; 0.5ms, 10-s train duration, supramaximal voltage, at various frequencies) under nonadrenergic noncholinergic conditions evoked muscular relaxation occasionally followed, at the higher stimulus frequencies, by rebound contractions. Inhibition of the synthesis of NO by Nω-nitro-L-arginine methyl ester (L-NAME; 100μM) virtually abolished the evoked relaxation. The relaxation was reduced also by apamin (0.1μM) and by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 1μM), a guanylyl cyclase inhibitor. The coadministration of apamin and ODQ produced additive effects on the responses to EFS. Sodium nitroprusside (0.1-100μM) produced a concentration-dependent reduction of the phasic spontaneous activity and at the highest dose used suppressed phasic activity and induced muscular relaxation. These effects were tetrodotoxin and L-NAME resistant and were antagonized both by apamin and by ODQ. 8-Bromoguanosine 3′,5′-cyclic monophosphate (0.1-100μM) reduced in a concentration-dependent manner the spontaneous mechanical activity and at 100μM suppressed the phasic activity and induced muscular relaxation, not antagonized by apamin. This study indicates that NO is the primary transmitter released by inhibitory nerves supplying the longitudinal muscle of mouse duodenum and that guanylate cyclase stimulation and opening of Ca2+-dependent K+ channels are independent mechanisms working in parallel to mediate NO action. {\circledC} 2002 Elsevier Science (USA). All rights reserved.",
keywords = "Biochemistry, Cyclic GMP, K+ -channels, Molecular Biology, Mouse duodenum, Nitric oxide, Nonadrenergic noncholinergic relaxation",
author = "Zizzo, {Maria Grazia} and Flavia Mule' and Serio, {Rosa Maria}",
year = "2003",
language = "English",
volume = "8",
pages = "48--52",
journal = "Nitric Oxide - Biology and Chemistry",
issn = "1089-8603",
publisher = "Academic Press Inc.",

}

TY - JOUR

T1 - Nitric oxide induces muscular relaxation via cyclic GMP-dependent and -independent mechanisms in the longitudinal muscle of the mouse duodenum

AU - Zizzo, Maria Grazia

AU - Mule', Flavia

AU - Serio, Rosa Maria

PY - 2003

Y1 - 2003

N2 - The aim of this study was to investigate, in mouse duodenum, the role of nitric oxide (NO) in the relaxation of longitudinal muscle evoked by nerve activation and the coupled action mechanism. Electrical field stimulation (EFS; 0.5ms, 10-s train duration, supramaximal voltage, at various frequencies) under nonadrenergic noncholinergic conditions evoked muscular relaxation occasionally followed, at the higher stimulus frequencies, by rebound contractions. Inhibition of the synthesis of NO by Nω-nitro-L-arginine methyl ester (L-NAME; 100μM) virtually abolished the evoked relaxation. The relaxation was reduced also by apamin (0.1μM) and by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 1μM), a guanylyl cyclase inhibitor. The coadministration of apamin and ODQ produced additive effects on the responses to EFS. Sodium nitroprusside (0.1-100μM) produced a concentration-dependent reduction of the phasic spontaneous activity and at the highest dose used suppressed phasic activity and induced muscular relaxation. These effects were tetrodotoxin and L-NAME resistant and were antagonized both by apamin and by ODQ. 8-Bromoguanosine 3′,5′-cyclic monophosphate (0.1-100μM) reduced in a concentration-dependent manner the spontaneous mechanical activity and at 100μM suppressed the phasic activity and induced muscular relaxation, not antagonized by apamin. This study indicates that NO is the primary transmitter released by inhibitory nerves supplying the longitudinal muscle of mouse duodenum and that guanylate cyclase stimulation and opening of Ca2+-dependent K+ channels are independent mechanisms working in parallel to mediate NO action. © 2002 Elsevier Science (USA). All rights reserved.

AB - The aim of this study was to investigate, in mouse duodenum, the role of nitric oxide (NO) in the relaxation of longitudinal muscle evoked by nerve activation and the coupled action mechanism. Electrical field stimulation (EFS; 0.5ms, 10-s train duration, supramaximal voltage, at various frequencies) under nonadrenergic noncholinergic conditions evoked muscular relaxation occasionally followed, at the higher stimulus frequencies, by rebound contractions. Inhibition of the synthesis of NO by Nω-nitro-L-arginine methyl ester (L-NAME; 100μM) virtually abolished the evoked relaxation. The relaxation was reduced also by apamin (0.1μM) and by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 1μM), a guanylyl cyclase inhibitor. The coadministration of apamin and ODQ produced additive effects on the responses to EFS. Sodium nitroprusside (0.1-100μM) produced a concentration-dependent reduction of the phasic spontaneous activity and at the highest dose used suppressed phasic activity and induced muscular relaxation. These effects were tetrodotoxin and L-NAME resistant and were antagonized both by apamin and by ODQ. 8-Bromoguanosine 3′,5′-cyclic monophosphate (0.1-100μM) reduced in a concentration-dependent manner the spontaneous mechanical activity and at 100μM suppressed the phasic activity and induced muscular relaxation, not antagonized by apamin. This study indicates that NO is the primary transmitter released by inhibitory nerves supplying the longitudinal muscle of mouse duodenum and that guanylate cyclase stimulation and opening of Ca2+-dependent K+ channels are independent mechanisms working in parallel to mediate NO action. © 2002 Elsevier Science (USA). All rights reserved.

KW - Biochemistry

KW - Cyclic GMP

KW - K+ -channels

KW - Molecular Biology

KW - Mouse duodenum

KW - Nitric oxide

KW - Nonadrenergic noncholinergic relaxation

UR - http://hdl.handle.net/10447/199039

M3 - Article

VL - 8

SP - 48

EP - 52

JO - Nitric Oxide - Biology and Chemistry

JF - Nitric Oxide - Biology and Chemistry

SN - 1089-8603

ER -