Modulation of electrically evoked responses in rat duodenum by activation of nicotinic cholinoceptors.
1. The effect of activation of nicotinic cholinoceptors in rat duodenal segments following electrical field stimulation (EFS) was investigated. 2. Electrical field stimulation elicited a two-component response: transient relaxation followed by contraction. The EFS-evoked response was tetrodotoxin (TTX; 1 mumol/L) sensitive. The relaxation component was NG-nitro-L-arginine (L-NNA; 100 mumol/L) sensitive, while the contractile response was atropine (1 mumol/L) sensitive. 3. 1,1-Dimethyl-4-phenyl-piperazinium iodide (DMPP; 20 mumol/L) induced relaxation of spontaneously active preparations that was L-NNA sensitive. L-Arginine (1 mmol/L) reversed the effects of L-NNA on DMPP-induced relaxation. 4. When EFS was applied, DMPP increased the amplitude of the relaxation component of the response and reduced the contractile component. 5. In the presence of L-NNA, the effect of DMPP on the relaxation component of the response to EFS was reduced, but the contractile response was not affected. L-Arginine partly reduced this effect of L-NNA. 6. Neither propranolol (1 mumol/L) nor yohimbine (1 mumol/L) had any effect on the actions of DMPP on EFS-evoked responses, but prazosin (1 mumol/L) strongly reduced the effect of DMPP on the contractile component of the response to EFS and slightly reduced the effect of DMPP on the relaxation response. 7. Histochemical studies demonstrated that, in the myenteric plexus of the rat duodenum, there are many reduced nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d)-positive neurons and that their number decreased after treatment with L-NNA. In the presence of L-arginine and L-NNA, the number of NADPH-d-positive neurons was similar to that found in control samples. 8. The data suggest that activation of nicotinic cholinoceptors modulates EFS-evoked responses in the rat duodenum as a result of the potentiation of nitrergic and adrenergic neurotransmission.
Sotirov
E S
ES
Institute of Physiology, Bulgarian Academy of Sciences, Sofia, Bulgaria. sotyo@iph.bio.acad.bg
Itzev
D E
DE
Papasova
M P
MP
D000200:Action Potentials / Q000187:drug effects; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D004246:Dimethylphenylpiperazinium Iodide / Q000494:pharmacology; D004386:Duodenum / Q000187:drug effects* / Q000294:innervation / Q000473:pathology; D004558:Electric Stimulation; D006651:Histocytochemistry; D008297:Male; D018727:Muscarinic Antagonists / Q000494:pharmacology*; D009119:Muscle Contraction / Q000187:drug effects; D009126:Muscle Relaxation / Q000187:drug effects; D009130:Muscle, Smooth / Q000187:drug effects* / Q000502:physiology; D009197:Myenteric Plexus / Q000187:drug effects / Q000378:metabolism; D009249:NADP / Q000032:analysis; D018722:Nicotinic Agonists / Q000494:pharmacology*; D019335:Nitroarginine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D011978:Receptors, Nicotinic / Q000187:drug effects*; D009435:Synaptic Transmission / Q000187:drug effects; D013779:Tetrodotoxin / Q000494:pharmacology
D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D018727:Muscarinic Antagonists; D018722:Nicotinic Agonists; D011978:Receptors, Nicotinic; D019335:Nitroarginine; D013779:Tetrodotoxin; D009249:NADP; D004246:Dimethylphenylpiperazinium Iodide; D001285:Atropine