Different regulatory effects of hydrogen sulfide and nitric oxide on gastric motility in mice
Male
Nitroprusside
Mice, Inbred ICR
0303 health sciences
Nitric Oxide Synthase Type III
Stomach
Cystathionine gamma-Lyase
Glycine
Aminooxyacetic Acid
Cystathionine beta-Synthase
Nitric Oxide Synthase Type II
Muscle, Smooth
Nitric Oxide
Mice
03 medical and health sciences
NG-Nitroarginine Methyl Ester
Alkynes
Animals
Nitric Oxide Donors
Hydrogen Sulfide
Gastrointestinal Motility
Muscle Contraction
DOI:
10.1016/j.ejphar.2013.10.017
Publication Date:
2013-10-21T12:45:54Z
AUTHORS (9)
ABSTRACT
NO and H2S are gaseous signaling molecules that modulate smooth muscle motility. We aimed to identify expressions of enzymes that catalyze H2S and NO generation in mouse gastric smooth muscle, and determine relationships between endogenous H2S and NO in regulation of smooth muscle motility. Western blotting and immunocytochemistry methods were used to track expressions of neuronal nitric oxide synthase (nNOS), endothelial nitric oxide synthase (eNOS), cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE) in gastric smooth muscles. Smooth muscle motility was recorded by isometric force transducers. cGMP production was measured by a specific radioimmunoassay. We found that CBS, CSE, eNOS, and nNOS were all expressed in mice gastric antral smooth muscle tissues, and in cultured gastric antral smooth muscle cells. AOAA significantly inhibited smooth muscle contractions in the gastric antrum, which was significantly recovered by NaHS, while PAG had no significant effect. l-NAME enhanced contractions. NaHS at low concentrations increased basal tension but decreased it at high concentrations. SNP significantly inhibited the contractions, which could be recovered by NaHS both in the absence and presence of CuSO4. ODQ did not block NaHS-induced excitatory effect, while IBMX partially blocked this effect. cGMP production in smooth muscle was significantly increased by SNP but was not affected by NaHS. All these results suggest that endogenous H2S and NO appear to play opposite roles in regulating gastric motility and their effects may be via separate signal transduction pathways. Intracellular H2S/NO levels may be maintained in a state of balance to warrant normal smooth muscle motility.
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