Modulation of slow waves by transmural nerve stimulation of smooth muscle tissue isolated from the corpus of the guinea-pig stomach.
Modulation of slow waves in response to transmural nerve stimulation (TNS) was investigated in smooth muscle preparations isolated from the corpus of the guinea-pig stomach. Single TNS evoked an inhibitory junction potential (i.j.p.) and enhanced the amplitude of the following slow wave. Effects of atropine, N(omega)-nitro-L-arginine (L-NA) and apamin revealed that corpus smooth muscle was innervated by cholinergic excitatory, nitrergic inhibitory and apamin-sensitive inhibitory nerves. In preparations isolated from the upper corpus which generated slow waves of 5-15 mV amplitude, a 1 min train of TNS (0.5 or 1 Hz frequency) increased the amplitude, with further enhancement by L-NA, but inhibition by atropine. In the lower corpus, larger amplitude (20-30 mV) slow waves were generated but these were not altered by a TNS train. However, application of L-NA and neostigmine, or often L-NA alone, resulted in increased frequency and decreased amplitude of slow waves during TNS, with an associated depolarization of the membrane. These changes were inhibited by atropine. In the presence of atropine, TNS reduced slow wave amplitude in an L-NA-sensitive manner. Acetylcholine (ACh) at 1 nM increased the amplitude of slow waves in the upper corpus. In the lower corpus, while low concentrations of ACh (<10 nM) did not increase the frequency and decrease the amplitude of slow waves with an associated depolarization of the membrane, this occurred at high concentrations of ACh (>10 nM). Application of the NO donor, sodium nitroprusside (SNP, 10 nM-1 microM), reduced the amplitude of slow waves. The changes in amplitude of slow waves elicited by ACh or SNP were not associated with a significant change in frequency. These results indicate that in the corpus circular smooth muscle, neural modulation of slow waves appeared to be exerted mainly on the amplitude, but not on the frequency.
Tanaka
Chiharu
C
Department of Physiology, Nagoya City University Medical School, Mizuho-ku, Nagoya 467-8601, Japan.
Domae
Kazumasa
K
Hashitani
Hikaru
H
Suzuki
Hikaru
H
D000109:Acetylcholine / Q000494:pharmacology / Q000502:physiology; D000818:Animals; D001030:Apamin / Q000494:pharmacology; D001285:Atropine / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects*; D009119:Muscle Contraction / Q000187:drug effects*; D009130:Muscle, Smooth / Q000187:drug effects* / Q000294:innervation*; D009388:Neostigmine / Q000494:pharmacology; D009433:Neural Inhibition / Q000187:drug effects; D020030:Nitric Oxide Donors / Q000494:pharmacology; D019335:Nitroarginine / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D013270:Stomach / Q000187:drug effects* / Q000294:innervation*
D020030:Nitric Oxide Donors; D009599:Nitroprusside; D019335:Nitroarginine; D001030:Apamin; D009388:Neostigmine; D001285:Atropine; D000109:Acetylcholine