Responses evoked by electrical stimulation, adenosine triphosphate, adenosine and 4-aminopyridine in taenia caeci of the guinea-pig.
Electrical stimulation of the guinea-pig taenia caeci (5 Hz, 2 s) caused enhancement of the [3H]purine flux from [3H]adenosine pools, accompanied by hyperpolarization (inhibitory junction potential) and relaxation of the muscle cells (35 degrees C). Interaction with receptors sensitive to catecholamines and acetylcholine was prevented by phentolamine (10(-6)M), propranolol (10(-6)M) and atropine (10(-6)M, respectively. The hyperpolarization and relaxation were completely inhibited by tetrodotoxin (TTX; 3 X 10(-7)M) but a substantial part of the [3H]purine flux persisted. The flux from the [3H]purine pool, from the [3H]methylcholine pool and from the noradrenaline pool was enhanced in the presence of 4-aminopyridine (3 X 10(-4)M; 4-AP), known to facilitate transmitter release. The release from the [3H]methylcholine pool was limited by hemicholinium (HC-3; 5 X 10(-4) M) and the release of noradrenaline was limited by reserpine (5 mg/kg; 24 h). The excess release of [3H]purine caused by 4-AP was completely abolished in the presence of TTX in preparations treated with HC-3 and reserpine. Addition of 4-AP to the Krebs solution evoked contraction of the smooth muscle cells. This response was abolished in the presence of HC-3 or atropine. The relaxation was also observed in reserpinized preparations in the presence of HC-3 and was not inhibited by either phentolamine or propranolol but was abolished in the presence of TTX. Hyperpolarization and suppression of spike activity accompanied the relaxation induced by 4-AP in reserpinized preparations treated with HC-3. Comparable responses were evoked by electrical stimulation of taenia caeci, by adenosine triphosphate (4 X 10(-4) M; ATP) and by adenosine (4 X 10(-4) M) in these experimental conditions. These responses evoked by electrical stimulation and by ATP were reversed in the presence of apamin (3 X 10(-7) M); the effect was reflected by an increased spike activity and contraction of the muscle cells in contrast to the adenosine response.(ABSTRACT TRUNCATED AT 250 WORDS)
Den Hertog
A
A
Pielkenrood
J
J
Van den Akker
J
J
D015761:4-Aminopyridine; D000241:Adenosine / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000494:pharmacology; D000631:Aminopyridines / Q000494:pharmacology; D000818:Animals; D002432:Cecum / Q000294:innervation* / Q000502:physiology; D004558:Electric Stimulation; D005260:Female; D005769:Gastrointestinal Motility / Q000187:drug effects; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008297:Male; D009130:Muscle, Smooth / Q000502:physiology*; D018377:Neurotransmitter Agents; D011687:Purines / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects
D000631:Aminopyridines; D018377:Neurotransmitter Agents; D011687:Purines; D000255:Adenosine Triphosphate; D015761:4-Aminopyridine; D000241:Adenosine