title: Hyperpolarization-induced dilatation of submucosal arterioles in the guinea-pig ileum.
abstract: 1. The effects of inhibition of acetylcholine (ACh)-induced hyperpolarization on dilatation of submucosal arterioles were investigated in the guinea-pig ileum. 2. In smooth muscles of the arterioles depolarized by Ba(2+) (0.5 mM) to about -40 mV, ACh (3 microM) repolarized the membrane to about -65 mV (hyperpolarization), irrespective of the absence or presence of L-N(omega)-nitroarginine (L-NOARG, 0.1 mM) and diclofenac (1 microM), and increased the diameter (dilatation). 3. Combined application of charybdotoxin (CTX, 50 nM) and apamin (0.1 microM), inhibitors of some types of K(+)-channels, abolished the ACh-induced hyperpolarization and dilatation. 4. 18 beta-Glycerrhetinic acid (18 beta-GA, 30 microM), a known inhibitor of gap junctions, depolarized the membrane to about -36 mV, either in the absence or in the presence of Ba(2+), with no associated contraction of the arterioles. In the presence of 18 beta-GA, ACh-induced hyperpolarization was abolished, however the dilatation was inhibited only partially, with associated inhibition of constriction produced by Ba(2+) and NA. 5. 18 beta-GA inhibited the dilatation produced by sodium nitroprusside, an NO donor. 6. The ACh-induced hyperpolarization and dilatation were abolished in the presence of 2-aminoethoxydiphenyl borate (30 microM), an inhibitory modulator of inositol trisphosphate receptor-mediated Ca(2+) release from intracellular stores. 7. It is concluded that in submucosal arterioles, hyperpolarizations produced by ACh have causal relationship to the arteriolar dilatation. 18 beta-GA did not induce parallel relationship between hyperpolarization and dilatation produced by ACh. 18 beta-GA may have unidentified inhibitory effects on agonist-mediated actions, in addition to the inhibition of gap junctions.
authors.affiliation: Department of Physiology, Nagoya City University Medical School, Mizuho-ku, Nagoya 467-8601, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Imaeda
authors.forename: Y
authors.initials: Y
authors.lastname: Yamamoto
authors.forename: H
authors.initials: H
authors.lastname: Fukuta
authors.forename: M
authors.initials: M
authors.lastname: Koshita
authors.forename: H
authors.initials: H
authors.lastname: Suzuki
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology*; D000287:Administration, Topical; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001030:Apamin / Q000494:pharmacology; D001160:Arterioles / Q000187:drug effects / Q000502:physiology; D001896:Boron Compounds / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D018999:Charybdotoxin / Q000494:pharmacology; D006034:Glycyrrhetinic Acid / Q000031:analogs & derivatives / Q000494:pharmacology*; D006168:Guinea Pigs; D007082:Ileum / Q000098:blood supply* / Q000187:drug effects; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000502:physiology; D026902:Potassium Channel Blockers; D014664:Vasodilation / Q000187:drug effects* / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D000893:Anti-Inflammatory Agents; D001896:Boron Compounds; D026902:Potassium Channel Blockers; D014665:Vasodilator Agents; D018999:Charybdotoxin; D001030:Apamin; C109986:2-aminoethoxydiphenyl borate; D000109:Acetylcholine; D006034:Glycyrrhetinic Acid; D002118:Calcium