Purinergic control of the quail rectum: modulation of adenosine 5'-triphosphate-mediated contraction with acetylcholine.
Electrical field stimulation (EFS) induces frequency-dependent contractions of the longitudinal muscle of isolated quail rectum which were sensitive to tetrodotoxin. The aim of the present study was to investigate whether purinergic neurons are implicated in the response to nerve stimulation. The shape of the EFS-induced contractile response was different depending on stimulus frequency; low frequencies (0.5-2 Hz) induced fast monophasic contractions with a small subsequent relaxation; whereas higher frequencies (5-50 Hz) induced biphasic contractile response that comprised fast initial component (as in case of low frequency) and a slow delayed contractile component in addition to the relaxation that follows the fast contractile component. Prior application of atropine (10 microM) completely abolished the slow delayed component but significantly enhanced the fast initial contractile component. Physostigmine (1-10 microM) significantly enhanced the slow delayed component with an inhibitory effect on the initial fast component. The nonspecific purinergic receptor antagonist, suramin (100-500 microM) significantly inhibited the fast initial contractile component with no significant effect on the slow delayed one. Complete blockade of the fast component was achieved by prior application of a combination consisted of suramin (50 microM) and pyridoxicalphosphate-6-azophenyl 2',4'-disulphonic acid tetrasodium (PPADS; 10 microM). Exogenous applications of adenosine 5'-triphosphate and acetylcholine (10 microM each), produced contractile responses that mimicked those induced by EFS. These data suggest that ATP is the main noncholinergic excitatory transmitter controlling the contractile activity of the quail rectum; and that its action could be modulated by acetylcholine.
Shiina
T
T
Department of Veterinary Medicine, Faculty of Applied Biological Sciences, Gifu University, Gifu 501-1193, Japan.
El-Mahmoudy
A
A
Khalifa
M
M
Draid
M
M
Shimizu
Y
Y
Takewaki
T
T
D000109:Acetylcholine / Q000494:pharmacology / Q000502:physiology*; D000255:Adenosine Triphosphate / Q000502:physiology*; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D002800:Cholinesterase Inhibitors / Q000494:pharmacology; D003370:Coturnix / Q000502:physiology*; D004558:Electric Stimulation; D005260:Female; D066298:In Vitro Techniques; D008297:Male; D018727:Muscarinic Antagonists / Q000494:pharmacology; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology*; D010830:Physostigmine / Q000494:pharmacology; D058914:Purinergic Antagonists; D011732:Pyridoxal Phosphate / Q000031:analogs & derivatives / Q000494:pharmacology; D011983:Receptors, Purinergic / Q000502:physiology*; D012007:Rectum / Q000502:physiology*; D013498:Suramin / Q000494:pharmacology
D002800:Cholinesterase Inhibitors; D018727:Muscarinic Antagonists; D058914:Purinergic Antagonists; D011983:Receptors, Purinergic; C077792:pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid; D011732:Pyridoxal Phosphate; D013498:Suramin; D001285:Atropine; D000255:Adenosine Triphosphate; D010830:Physostigmine; D000109:Acetylcholine