Role of Ca2+-activated K+ channels in acetylcholine-induced dilatation of the basilar artery in vivo

Takanari Kitazono, Setsuro Ibayashi, Tetsuhiko Nagao, Kenichiro Fujii, Masatoshi Fujishima

研究成果: ジャーナルへの寄稿記事

13 引用 (Scopus)

抄録

1. We tested the hypothesis that activation of large conductance calcium-activated potassium channels is involved in dilator responses of the basilar artery to acetylcholine in vivo. Using a cranial window in anaesthetized rats, we examined responses of the basilar artery to acetylcholine. 2. Topical application of acetylcholine (10-6 and 10-5 M) increased diameter of the basilar artery from 238 ± 7 μm to 268 ± 7 and 288 ± 7 μm, respectively (P < 0.05 vs. baseline diameter). Iberiotoxin (10-8 M), an inhibitor of large conductance calcium-activated potassium channels, did not affect baseline diameter of the basilar artery. In the presence of 10-8 M iberiotoxin, 10-6 and 10-5 M acetylcholine increased diameter of the basilar artery from 239 ± 7 μm to 246 ± 7 and 261 ± 7 μm, respectively. Thus, iberiotoxin attenuated acetylcholine-induced dilatation of the basilar artery (P < 0.05). 3. Sodium nitroprusside (10-7 and 10-6 M) increased diameter of the basilar artery from 242 ± 9 μm to 310 ± 12 and 374 ± 13 μm, respectively (P < 0.05 vs. baseline diameter). In the presence of iberiotoxin (10-8 M), sodium nitroprusside (10-7 and 10-6 M) increased diameter of the basilar artery from 243 ± 6 μm to 259 ± 9 and 311 ± 12 μm, respectively. Thus, iberiotoxin attenuated dilator responses of the basilar artery to sodium nitroprusside (P < 0.05). 4. Iberiotoxin partly inhibited dilator responses of the basilar artery to forskolin, a direct activator of adenylate cyclase, but did not affect vasodilatation produced by levcromakalim, a potassium channel opener. 5. These results suggest that dilator responses of the basilar artery to acetylcholine and sodium nitroprusside are mediated, in part, by activation of large conductance calcium-activated potassium channels. Because both acetylcholine and sodium nitroprusside have been shown to activate guanylate cyclase via nitric oxide, activation of large conductance calcium-activated potassium channels may be one of the major mechanisms by which eyelid GMP causes dilatation of the basilar artery in vivo.

元の言語英語
ページ(範囲)102-106
ページ数5
ジャーナルBritish Journal of Pharmacology
120
発行部数1
DOI
出版物ステータス出版済み - 2 1 1997

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Calcium-Activated Potassium Channels
Basilar Artery
Acetylcholine
Dilatation
Large-Conductance Calcium-Activated Potassium Channels
Nitroprusside
Cromakalim
Guanylate Cyclase
Potassium Channels
Colforsin
Eyelids
Adenylyl Cyclases
Vasodilation
iberiotoxin
Nitric Oxide

All Science Journal Classification (ASJC) codes

  • Pharmacology

これを引用

Role of Ca2+-activated K+ channels in acetylcholine-induced dilatation of the basilar artery in vivo. / Kitazono, Takanari; Ibayashi, Setsuro; Nagao, Tetsuhiko; Fujii, Kenichiro; Fujishima, Masatoshi.

:: British Journal of Pharmacology, 巻 120, 番号 1, 01.02.1997, p. 102-106.

研究成果: ジャーナルへの寄稿記事

Kitazono, Takanari ; Ibayashi, Setsuro ; Nagao, Tetsuhiko ; Fujii, Kenichiro ; Fujishima, Masatoshi. / Role of Ca2+-activated K+ channels in acetylcholine-induced dilatation of the basilar artery in vivo. :: British Journal of Pharmacology. 1997 ; 巻 120, 番号 1. pp. 102-106.
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abstract = "1. We tested the hypothesis that activation of large conductance calcium-activated potassium channels is involved in dilator responses of the basilar artery to acetylcholine in vivo. Using a cranial window in anaesthetized rats, we examined responses of the basilar artery to acetylcholine. 2. Topical application of acetylcholine (10-6 and 10-5 M) increased diameter of the basilar artery from 238 ± 7 μm to 268 ± 7 and 288 ± 7 μm, respectively (P < 0.05 vs. baseline diameter). Iberiotoxin (10-8 M), an inhibitor of large conductance calcium-activated potassium channels, did not affect baseline diameter of the basilar artery. In the presence of 10-8 M iberiotoxin, 10-6 and 10-5 M acetylcholine increased diameter of the basilar artery from 239 ± 7 μm to 246 ± 7 and 261 ± 7 μm, respectively. Thus, iberiotoxin attenuated acetylcholine-induced dilatation of the basilar artery (P < 0.05). 3. Sodium nitroprusside (10-7 and 10-6 M) increased diameter of the basilar artery from 242 ± 9 μm to 310 ± 12 and 374 ± 13 μm, respectively (P < 0.05 vs. baseline diameter). In the presence of iberiotoxin (10-8 M), sodium nitroprusside (10-7 and 10-6 M) increased diameter of the basilar artery from 243 ± 6 μm to 259 ± 9 and 311 ± 12 μm, respectively. Thus, iberiotoxin attenuated dilator responses of the basilar artery to sodium nitroprusside (P < 0.05). 4. Iberiotoxin partly inhibited dilator responses of the basilar artery to forskolin, a direct activator of adenylate cyclase, but did not affect vasodilatation produced by levcromakalim, a potassium channel opener. 5. These results suggest that dilator responses of the basilar artery to acetylcholine and sodium nitroprusside are mediated, in part, by activation of large conductance calcium-activated potassium channels. Because both acetylcholine and sodium nitroprusside have been shown to activate guanylate cyclase via nitric oxide, activation of large conductance calcium-activated potassium channels may be one of the major mechanisms by which eyelid GMP causes dilatation of the basilar artery in vivo.",
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AU - Fujishima, Masatoshi

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N2 - 1. We tested the hypothesis that activation of large conductance calcium-activated potassium channels is involved in dilator responses of the basilar artery to acetylcholine in vivo. Using a cranial window in anaesthetized rats, we examined responses of the basilar artery to acetylcholine. 2. Topical application of acetylcholine (10-6 and 10-5 M) increased diameter of the basilar artery from 238 ± 7 μm to 268 ± 7 and 288 ± 7 μm, respectively (P < 0.05 vs. baseline diameter). Iberiotoxin (10-8 M), an inhibitor of large conductance calcium-activated potassium channels, did not affect baseline diameter of the basilar artery. In the presence of 10-8 M iberiotoxin, 10-6 and 10-5 M acetylcholine increased diameter of the basilar artery from 239 ± 7 μm to 246 ± 7 and 261 ± 7 μm, respectively. Thus, iberiotoxin attenuated acetylcholine-induced dilatation of the basilar artery (P < 0.05). 3. Sodium nitroprusside (10-7 and 10-6 M) increased diameter of the basilar artery from 242 ± 9 μm to 310 ± 12 and 374 ± 13 μm, respectively (P < 0.05 vs. baseline diameter). In the presence of iberiotoxin (10-8 M), sodium nitroprusside (10-7 and 10-6 M) increased diameter of the basilar artery from 243 ± 6 μm to 259 ± 9 and 311 ± 12 μm, respectively. Thus, iberiotoxin attenuated dilator responses of the basilar artery to sodium nitroprusside (P < 0.05). 4. Iberiotoxin partly inhibited dilator responses of the basilar artery to forskolin, a direct activator of adenylate cyclase, but did not affect vasodilatation produced by levcromakalim, a potassium channel opener. 5. These results suggest that dilator responses of the basilar artery to acetylcholine and sodium nitroprusside are mediated, in part, by activation of large conductance calcium-activated potassium channels. Because both acetylcholine and sodium nitroprusside have been shown to activate guanylate cyclase via nitric oxide, activation of large conductance calcium-activated potassium channels may be one of the major mechanisms by which eyelid GMP causes dilatation of the basilar artery in vivo.

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