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This study explored the role and mechanism of Ca<jats:sup>2+<\/jats:sup> handling in coronary artery dysfunction in type 2 diabetic rats. Zucker diabetic fatty (ZDF) rats were used as the type 2 diabetes mellitus model. The contractility of coronary artery rings induced by KCl, CaCl<jats:sub>2<\/jats:sub>, 5\u2010HT and U46619 was significantly lower in ZDF rats than in Zucker lean rats. Vasoconstriction induced by 5\u2010HT and U46619 was greatly inhibited by nifedipine. However, in the presence of 1\u00a0\u03bcM nifedipine or in the Ca<jats:sup>2+<\/jats:sup>\u2010free KH solution containing 1\u00a0\u03bcM nifedipine, there was no difference in the vasoconstriction between Zucker lean and ZDF rats. Store\u2010operated calcium channels (SOCs) were not involved in coronary vasoconstriction. The downregulation of contractile proteins and the upregulation of synthesized proteins were in coronary artery smooth muscle cells (CASMCs) from ZDF rats. Metformin reversed the reduction of vasoconstriction in ZDF rats. 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