Centrally Applied Nitric Oxide Donors Inhibit Vagally Evoked Rat Gastric Acid Secretion: Involvement of Sympathetic Outflow

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Author(s)

Abstract

Intracerebroventricularly (i.c.v.)administered nitric oxide (NO)donors, 3-morpholinosydnonimine (SIN-1)(100-500 μg/animal)and sodium nitroprusside (SNP)(100-250 μg/animal)dosedependently inhibited the rat gastric acid secretion evoked by vagal stimulation at 3 Hz. Furthermore, the inhibitory effect of SIN-1 (250 μg/animal)was more marked and its onset was more rapid than that of SNP (250 μg/animal). The SIN-1 (250 μg/animal)-induced antisecretory effect was abolished by both splanchnicotomy and phentolamine (5 mg/kg, i.m.), and also by indomethacin (500 μg/animal, i.c.v.). These results suggest that i.c.v. administered NO donors inhibit vagally evoked gastric acid secretion by activation of central sympathetic outflow. Central prostaglandin is probably implicated in this NOmediated antisecretory effect.

Journal

  • The Japanese Journal of Pharmacology

    The Japanese Journal of Pharmacology 74(4), 337-340, 1997-08-01

    The Japanese Pharmacological Society

References:  15

Cited by:  1

Codes

  • NII Article ID (NAID)
    10008679557
  • NII NACSIS-CAT ID (NCID)
    AA00691188
  • Text Lang
    ENG
  • Article Type
    Journal Article
  • ISSN
    00215198
  • NDL Article ID
    4287830
  • NDL Source Classification
    ZS51(科学技術--薬学)
  • NDL Call No.
    Z53-D199
  • Data Source
    CJP  CJPref  NDL  J-STAGE 
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