File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Kaempferol enhances endothelium-dependent relaxation in the porcine coronary artery through activation of large-conductance Ca2+ -activated K+ channels

TitleKaempferol enhances endothelium-dependent relaxation in the porcine coronary artery through activation of large-conductance Ca2+ -activated K+ channels
Authors
Issue Date2015
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1
Citation
British Journal of Pharmacology, 2015, v. 172 n. 12, p. 3003-3014 How to Cite?
AbstractBACKGROUND AND PURPOSE: Kaempferol, a plant flavonoid present in normal human diet, can modulate vasomotor tone. The present study aimed to elucidate the signalling pathway through which this flavonoid enhanced relaxation of vascular smooth muscle. EXPERIMENTAL APPROACH: The effect of kaempferol on the relaxation of porcine coronary arteries to endothelium-dependent (bradykinin) and -independent (sodium nitroprusside) relaxing agents was studied in an in vitro organ chamber setup. The whole-cell patch-clamp technique was used to determine the effect of kaempferol on potassium channels in porcine coronary artery smooth muscle cells (PCASMCs). KEY RESULTS: At a concentration without direct effect on vascular tone, kaempferol (3 × 10(-6)  M) enhanced relaxations produced by bradykinin and sodium nitroprusside. The potentiation by kaempferol of the bradykinin-induced relaxation was not affected by N(ω) -nitro-L-arginine methyl ester, an inhibitor of NO synthase (10(-4)  M) or TRAM-34 plus UCL 1684, inhibitors of intermediate- and small-conductance calcium-activated potassium channels, respectively (10(-6)  M each), but was abolished by tetraethylammonium chloride, a non-selective inhibitor of calcium-activated potassium channels (10(-3)  M), and iberiotoxin, a selective inhibitor of large-conductance calcium-activated potassium channel (KCa 1.1; 10(-7)  M). Iberiotoxin also inhibited the potentiation by kaempferol of sodium nitroprusside-induced relaxations. Kaempferol stimulated an outward-rectifying current in PCASMCs, which was abolished by iberiotoxin. CONCLUSIONS AND IMPLICATIONS: The present results suggest that, in smooth muscle cells of the porcine coronary artery, kaempferol enhanced relaxations caused by endothelium-derived and exogenous NO as well as those due to endothelium-dependent hyperpolarization. This vascular effect of kaempferol involved the activation of KCa 1.1 channels. © 2015 The British Pharmacological Society.
Persistent Identifierhttp://hdl.handle.net/10722/211891
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorXu, YC-
dc.contributor.authorLeung, SWS-
dc.contributor.authorLeung, GPH-
dc.contributor.authorMan, RYK-
dc.date.accessioned2015-07-21T02:15:06Z-
dc.date.available2015-07-21T02:15:06Z-
dc.date.issued2015-
dc.identifier.citationBritish Journal of Pharmacology, 2015, v. 172 n. 12, p. 3003-3014-
dc.identifier.issn0007-1188-
dc.identifier.urihttp://hdl.handle.net/10722/211891-
dc.description.abstractBACKGROUND AND PURPOSE: Kaempferol, a plant flavonoid present in normal human diet, can modulate vasomotor tone. The present study aimed to elucidate the signalling pathway through which this flavonoid enhanced relaxation of vascular smooth muscle. EXPERIMENTAL APPROACH: The effect of kaempferol on the relaxation of porcine coronary arteries to endothelium-dependent (bradykinin) and -independent (sodium nitroprusside) relaxing agents was studied in an in vitro organ chamber setup. The whole-cell patch-clamp technique was used to determine the effect of kaempferol on potassium channels in porcine coronary artery smooth muscle cells (PCASMCs). KEY RESULTS: At a concentration without direct effect on vascular tone, kaempferol (3 × 10(-6)  M) enhanced relaxations produced by bradykinin and sodium nitroprusside. The potentiation by kaempferol of the bradykinin-induced relaxation was not affected by N(ω) -nitro-L-arginine methyl ester, an inhibitor of NO synthase (10(-4)  M) or TRAM-34 plus UCL 1684, inhibitors of intermediate- and small-conductance calcium-activated potassium channels, respectively (10(-6)  M each), but was abolished by tetraethylammonium chloride, a non-selective inhibitor of calcium-activated potassium channels (10(-3)  M), and iberiotoxin, a selective inhibitor of large-conductance calcium-activated potassium channel (KCa 1.1; 10(-7)  M). Iberiotoxin also inhibited the potentiation by kaempferol of sodium nitroprusside-induced relaxations. Kaempferol stimulated an outward-rectifying current in PCASMCs, which was abolished by iberiotoxin. CONCLUSIONS AND IMPLICATIONS: The present results suggest that, in smooth muscle cells of the porcine coronary artery, kaempferol enhanced relaxations caused by endothelium-derived and exogenous NO as well as those due to endothelium-dependent hyperpolarization. This vascular effect of kaempferol involved the activation of KCa 1.1 channels. © 2015 The British Pharmacological Society.-
dc.languageeng-
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1-
dc.relation.ispartofBritish Journal of Pharmacology-
dc.rightsBritish Journal of Pharmacology. Copyright © John Wiley & Sons Ltd.-
dc.titleKaempferol enhances endothelium-dependent relaxation in the porcine coronary artery through activation of large-conductance Ca2+ -activated K+ channels-
dc.typeArticle-
dc.identifier.emailLeung, SWS: swsleung@hku.hk-
dc.identifier.emailLeung, GPH: gphleung@hkucc.hku.hk-
dc.identifier.emailMan, RYK: rykman@hku.hk-
dc.identifier.authorityLeung, SWS=rp00235-
dc.identifier.authorityLeung, GPH=rp00234-
dc.identifier.authorityMan, RYK=rp00236-
dc.identifier.doi10.1111/bph.13108-
dc.identifier.pmid25652142-
dc.identifier.pmcidPMC4459019-
dc.identifier.hkuros244681-
dc.identifier.volume172-
dc.identifier.issue12-
dc.identifier.spage3003-
dc.identifier.epage3014-
dc.publisher.placeUnited Kingdom-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats