{"created":"2025-04-14T14:56:14.592909+00:00","id":2019500,"links":{},"metadata":{"_buckets":{"deposit":"2f8d4e8d-1a97-4ced-8ba1-028a125e883d"},"_deposit":{"id":"2019500","owners":[1],"pid":{"revision_id":0,"type":"depid","value":"2019500"},"status":"published"},"_oai":{"id":"oai:teikyo-u.repo.nii.ac.jp:02019500","sets":["1726879085919:1741828256493"]},"author_link":[],"item_1551264308487":{"attribute_name":"Title","attribute_value_mlt":[{"subitem_title":"Differential blocking action of dihydropyridine Ca2+ antagonists on a T-type Ca2+ channel (α1G) expressed in Xenopus oocytes","subitem_title_language":"eng"}]},"item_1551264340087":{"attribute_name":"Creator","attribute_type":"creator","attribute_value_mlt":[{"familyNames":[{"familyName":"furukawa","familyNameLang":"eng"},{"familyName":"古川","familyNameLang":"jpn"}],"givenNames":[{"givenName":"taiji","givenNameLang":"eng"},{"givenName":"泰司","givenNameLang":"jpn"}]},{"familyNames":[{"familyName":"Nukada"}],"givenNames":[{"givenName":"Toshihide"}]},{"familyNames":[{"familyName":"Miura"}],"givenNames":[{"givenName":"Reiko"}]},{"familyNames":[{"familyName":"Ooga"}],"givenNames":[{"givenName":"Kyoji"}]},{"familyNames":[{"familyName":"Honda"}],"givenNames":[{"givenName":"Mituyoshi"}]},{"familyNames":[{"familyName":"Watanabe"}],"givenNames":[{"givenName":"Suguru"}]},{"familyNames":[{"familyName":"Koganesawa"}],"givenNames":[{"givenName":"Satoshi"}]},{"familyNames":[{"familyName":"Isshiki"}],"givenNames":[{"givenName":"Takaaki"}]}]},"item_1551264447183":{"attribute_name":"アクセス権","attribute_value_mlt":[{"subitem_access_right":"open access","subitem_access_right_uri":"http://purl.org/coar/access_right/c_abf2"}]},"item_1551264822581":{"attribute_name":"Subject","attribute_value_mlt":[{"subitem_subject":"Dihydropyridine","subitem_subject_language":"eng","subitem_subject_scheme":"Other"},{"subitem_subject":"T-type calcium channel","subitem_subject_language":"eng","subitem_subject_scheme":"Other"},{"subitem_subject":"Xenopus oocyte","subitem_subject_language":"eng","subitem_subject_scheme":"Other"},{"subitem_subject":"Pharmacology","subitem_subject_language":"eng","subitem_subject_scheme":"SciVal"},{"subitem_subject":"薬理学","subitem_subject_language":"jpn","subitem_subject_scheme":"SciVal"},{"subitem_subject":"Cardiology and Cardiovascular Medicine","subitem_subject_language":"eng","subitem_subject_scheme":"SciVal"},{"subitem_subject":"循環器および心血管医学","subitem_subject_language":"jpn","subitem_subject_scheme":"SciVal"}]},"item_1551264846237":{"attribute_name":"Description","attribute_value_mlt":[{"subitem_description":"

Recent reports show that efonidipine, a dihydropyridine Ca2+ antagonist, has blocking action on T-type Ca2+ channels, which may produce favorable actions on cardiovascular systems. However, the effects of other dihydropyridine Ca2+ antagonists on T-type Ca2+ channels have not been investigated yet. Therefore, in this study, we examined the effects of dihydropyridine compounds clinically used for treatment of hypertension on a T-type Ca2+ channel subtype, α1G, expressed in Xenopus oocytes. These effects were compared with those on T-type Ca2+ channel. Rabbit L-type (α1Cα2/ δβ1a) or rat T-type (α1G) Ca2+ channel was expressed in Xenopus oocytes by injection of cRNA for each subunit. The Ba2+ currents through expressed channels were measured by conventional 2-microelectrode voltage-clamp methods. Twelve DHPs (amlodipine, barnidipine, benidipine, cilnidipine, efonidipine, felodipine, manidipine, nicardipine, nifedipine, nilvadipine, nimodipine, nitrendipine) and mibefradil were tested. Cilnidipine, felodipine, nifedipine, nilvadipine, minodipine, and nitrendipine had little effect on the T-type channel. The blocks by drugs at 10 μM were less than 10% at a holding potential of -100 mV The remaining 6 drugs had blocking action on the T-type channel comparable to that on the L-type channel. The blocking actions were also comparable to that by mibefradil. These results show that many dihydropyridine Ca2+ antagonists have blocking action on the α1G channel subtype. The action of dihydropyridine Ca2+ antagonists in clinical treatment should be evaluated on the basis of subtype selectivity.

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