title: Serotonin depolarizes the membrane potential in rat mesenteric artery myocytes by decreasing voltage-gated K+ currents.
abstract: We hypothesized that voltage-gated K+ (Kv) currents regulate the resting membrane potential (Em), and that serotonin (5-HT) causes Em depolarization by reducing Kv currents in rat mesenteric artery smooth muscle cells (MASMCs). The resting Em was about -40 mV in the nystatin-perforated patch configuration, and the inhibition of Kv currents by 4-aminopyridine caused marked Em depolarization. The inhibition of Ca2+-activated K+ (KCa) currents had no effect on Em. 5-HT (1 microM) depolarized Em by approximately 11 mV and reduced the Kv currents to approximately 63% of the control at -20 mV. Similar 5-HT effects were observed with the conventional whole-cell configuration with a weak Ca2+ buffer in the pipette solution, but not with a strong Ca2+ buffer. In the presence of tetraethylammonium (1mM), 5-HT caused Em depolarization similar to the control condition. These results indicate that the resting Em is largely under the regulation of Kv currents in rat MASMCs, and that 5-HT depolarizes Em by reducing Kv currents in a [Ca2+]i-dependent manner.
authors.affiliation: Artificial Muscle Research Center, College of Medicine, Konkuk University 322 Danwol-dong, Choongju 380-701, Republic of Korea. ymbae30@kku.ac.kr
authors.forename: Young Min
authors.initials: YM
authors.lastname: Bae
authors.forename: Aeran
authors.initials: A
authors.lastname: Kim
authors.forename: Junghwan
authors.initials: J
authors.lastname: Kim
authors.forename: Sang Woong
authors.initials: SW
authors.lastname: Park
authors.forename: Tae-Kyung
authors.initials: TK
authors.lastname: Kim
authors.forename: Youn-Ri
authors.initials: YR
authors.lastname: Lee
authors.forename: Bokyung
authors.initials: B
authors.lastname: Kim
authors.forename: Sung Il
authors.initials: SI
authors.lastname: Cho
mesh_terms: D015761:4-Aminopyridine / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D002614:Chelating Agents / Q000494:pharmacology; D004533:Egtazic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D007476:Ionophores / Q000494:pharmacology; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D008638:Mesenteric Arteries / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D032342:Muscle Cells / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D009761:Nystatin / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D026902:Potassium Channel Blockers / Q000494:pharmacology; D024681:Potassium Channels, Calcium-Activated / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012701:Serotonin / Q000494:pharmacology*; D019789:Tetraethylammonium / Q000494:pharmacology
chemical_list: D002614:Chelating Agents; D007476:Ionophores; D026902:Potassium Channel Blockers; D024681:Potassium Channels, Calcium-Activated; D009761:Nystatin; D012701:Serotonin; D004533:Egtazic Acid; D019789:Tetraethylammonium; D000255:Adenosine Triphosphate; D015761:4-Aminopyridine; C025603:1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid; D002118:Calcium