title: Functional role of Ca(2+)-activated K+ channels in resting state of carotid arteries from SHR.
abstract: Carotid arteries from spontaneously hypertensive rats (SHR) exhibited an active tone when exposed to a physiological salt solution; that is, the tension decreased when nifedipine was added. To determine the possible role of Ca(2+)-activated K+ (KCa) channels in the resting state of these arteries, the effects of agents that interact with these channels on tension and 86Rb efflux were compared in endothelium-denuded strips of carotid arteries from SHR and normotensive Wistar-Kyoto rats (WKY). The addition of charybdotoxin, a blocker of high-conductance KCa channels, to the resting strips produced a concentration-dependent contraction in SHR but not in WKY. In resting strips preloaded with 86Rb, the basal 86Rb efflux rate constant was significantly greater in SHR than in WKY. The addition of nifedipine to the resting strips decreased the basal 86Rb efflux rate constant only in SHR. The effect of nifedipine on tension and 86Rb efflux in 25.9 mM K(+)-contracted strips of WKY was comparable to the effect of this blocker in the resting strips of SHR. The basal 45Ca influx in resting strips of SHR was significantly increased when compared with WKY, and this increase in SHR was abolished by nifedipine. These results suggest that the transmembrane Ca2+ influx via L-type voltage-dependent Ca2+ channels was significantly increased in the resting state of carotid arteries from SHR and that the KCa channels were highly activated.
authors.affiliation: Department of Pharmacology, Nagoya City University Medical School, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Asano
authors.forename: K
authors.initials: K
authors.lastname: Masuzawa-Ito
authors.forename: T
authors.initials: T
authors.lastname: Matsuda
authors.forename: Y
authors.initials: Y
authors.lastname: Imaizumi
authors.forename: M
authors.initials: M
authors.lastname: Watanabe
authors.forename: K
authors.initials: K
authors.lastname: Ito
mesh_terms: D000818:Animals; D002118:Calcium / Q000502:physiology*; D002339:Carotid Arteries / Q000187:drug effects / Q000502:physiology*; D018999:Charybdotoxin; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D009543:Nifedipine / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000502:physiology*; D051381:Rats; D011918:Rats, Inbred SHR; D017208:Rats, Wistar; D012413:Rubidium / Q000378:metabolism; D012604:Scorpion Venoms / Q000494:pharmacology; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D014661:Vasoconstriction
chemical_list: D026902:Potassium Channel Blockers; D015221:Potassium Channels; D012604:Scorpion Venoms; D013757:Tetraethylammonium Compounds; D018999:Charybdotoxin; D019789:Tetraethylammonium; D009543:Nifedipine; D012413:Rubidium; D011188:Potassium; D002118:Calcium