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1 Department of General Surgery, University Hospital, 72076 Tübingen, Germany; and 2 Department of Biomedical Science, University of Sheffield, Sheffield S10 2TN, United Kingdom
The concept of functional interaction between
mast cells and intestinal afferents is gaining support. We have
therefore characterized the action of histamine on jejunal afferent
discharge in the anesthetized rat. Whole nerve mesenteric afferent
discharge was recorded in conjunction with intestinal pressure in
response to a range of histamine agonists and antagonists. Histamine at
2, 4, and 8 µmol/kg (iv) evoked a dose-dependent biphasic increase in
afferent discharge together with a biphasic rise in intestinal
pressure. However, these two events were mediated independently, since
nifedipine (1 mg/kg) substantially reduced the intestinal pressure
increase but not the afferent discharge. These responses were
completely inhibited by pyrilamine (5 mg/kg) but unaffected by
ranitidine (5 mg/kg) or thioperamide (2 mg/kg). Neither the
selective H2 receptor agonist
dimaprit nor the selective H3
receptor agonist R-
-methylhistamine
caused any modulation of afferent discharge. We conclude that histamine
stimulates an H1 receptor-mediated increase in mesenteric afferent discharge that is independent of
intestinal motor events. This suggests that histamine potentially acts
as a mediator in mast cell-to-afferent nerve communication in the small
intestine.
intestine
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