@article{oai:hirosaki.repo.nii.ac.jp:00003664,
 author = {Hasegawa, Kazushi and Oikawa, Koichi and Yoshida, Ikko and Ishizaka, Hiroshi and Osanai, Tomohiro and Motomura, Shigeru and Okumura, Ken},
 issue = {1/2/3/4},
 journal = {弘前医学},
 month = {Mar},
 note = {application/pdf, To examine the effect of chronic hypertension on endothelium-derived hyperpolarizing factor（ EDHF）
responses, the hearts of Wistar-Kyoto rats（ WKY） and spontaneously hypertensive rats（ SHR） were isolated and
perfused using Langendorff system with constant perfusion pressure. Bradykinin increased coronary fl ow（ CF） dosedependently
and this was not aff ected by NG-nitro-L-arginine methyl ester or indomethacin, indicating that bradykinin’s
eff ect on CF was not mediated by nitric oxide or prostacyclin but by EDHF. Bradykinin-induced CF increase was smaller
in SHR than in WKY. Tetrabutylammonium（ a non-specific KCa channel blocker） abolished bradykinin-induced CF
increase in both rats. 1-Ethyl-2-benzimedazolinone（ 1-EBIO, an agonist of intermediate conductance KCa channel）-induced
increase in CF was smaller in SHR than in WKY. 1,3-Dihydro-1-[2-hydroxy-5（- trifl uoromethyl） phenyl]-5（- trifl uoromethyl）
-2H-benzimidazol-2-one（ NS1619, an agonist of large conductance KCa channel）-induced increase in CF did not differ
between SHR and WKY. In early stage of hypertension, there was no signifi cant diff erence between SHR and WKY in
bradykinin- and 1-EBIO-induced increases in CF. In conclusion, EDHF response in coronary microcirculation is impaired
in SHR due to dysfunction of intermediate-conductance calcium-activated potassium channels., 弘前医学. 60(1/2/3/4), 2009, p.86-95},
 pages = {86--95},
 title = {Impairment of Calcium-Activated Potassium Channels in Endothelium-Derived Hyperpolarizing Factor Responses in Spontaneously Hypertensive Rats},
 volume = {60},
 year = {2009}
}