The effects on net fluid transport of noxious stimulation of jejunal mucosa in anaesthetized rats.
A major aim of the present study was to investigate whether exposing the jejunal mucosa to a noxious stimulus induces a net fluid secretion by activating the enteric nervous system (ENS) and, if so, to what extent an axon reflex was involved. Net fluid transport was measured in vivo with a gravimetric method. The intestinal mucosa was exposed to an isotonic solution with an unphysiologically low pH (1.0). This evoked a fluid secretion, which was markedly attenuated by giving hexamethonium (nicotinic receptor antagonist) i.v. or exposing the intestinal serosa to lidocaine (local anaesthetic). Atropine (muscarinic receptor antagonist) had no effect. Luminal acid evoked a fluid secretion of the same magnitude in acutely denervated segments and in segments denervated about 3 weeks prior to the experiments. Luminal capsaicin (1.6-16 mM) did not influence jejunal net fluid transport. A second aim of the study is to investigate the effect of nifedipine (Ca channel blocker of L-type) on the acid-induced fluid secretion. Nifedipine markedly attenuated acid-induced fluid secretion. In contrast to cholera toxin-evoked secretion, the nifedipine effect was not mediated via 5 hydroxytryptamine (5-HT) as judged by measurements of 5-HT release into the intestinal lumen and the lack of effect of granisetron (5-HT3 receptor antagonist). It is concluded that the net fluid secretion evoked by hydrochloric acid in the small intestine is mainly mediated via an intramural reflex in the ENS. No experimental evidence was obtained for the involvement of an axon reflex. The site of action of the calcium channel blocker is tentatively discussed.
Timar Peregrin
A
A
Department of Physiology, Göteborg University, Sweden.
Svensson
M
M
Ahlman
H
H
Jodal
M
M
Lundgren
O
O
D000758:Anesthesia; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001369:Axons / Q000737:chemistry / Q000187:drug effects / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000502:physiology*; D002211:Capsaicin / Q000494:pharmacology; D017615:Enteric Nervous System / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D004759:Enterochromaffin Cells / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism; D005947:Glucose / Q000494:pharmacology; D017829:Granisetron / Q000494:pharmacology; D018738:Hexamethonium / Q000494:pharmacology; D006851:Hydrochloric Acid / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D006897:Hydroxyindoleacetic Acid / Q000378:metabolism; D007408:Intestinal Absorption / Q000187:drug effects* / Q000502:physiology; D007413:Intestinal Mucosa / Q000737:chemistry / Q000166:cytology / Q000378:metabolism; D007583:Jejunum / Q000166:cytology / Q000294:innervation / Q000378:metabolism*; D008297:Male; D018727:Muscarinic Antagonists / Q000494:pharmacology; D018733:Nicotinic Antagonists / Q000494:pharmacology; D009543:Nifedipine / Q000494:pharmacology; D019188:Organ Preservation Solutions / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012701:Serotonin / Q000378:metabolism; D012702:Serotonin Antagonists / Q000494:pharmacology; D013268:Stimulation, Chemical; D014325:Tromethamine / Q000494:pharmacology; D014867:Water / Q000378:metabolism*
D001285:Atropine; D002121:Calcium Channel Blockers; D015220:Calcium Channels; D002211:Capsaicin; D005947:Glucose; D017829:Granisetron; D018738:Hexamethonium; D006851:Hydrochloric Acid; D006897:Hydroxyindoleacetic Acid; D018727:Muscarinic Antagonists; D018733:Nicotinic Antagonists; D009543:Nifedipine; D019188:Organ Preservation Solutions; D012701:Serotonin; D012702:Serotonin Antagonists; D014325:Tromethamine; D014867:Water; C074097:Krebs-Henseleit solution