SummaryBackground-Metformin might reduce insulin requirement and improve glycaemia in patients with type 1 diabetes, but whether it has cardiovascular benefits is unknown. We aimed to investigate whether metformin treatment (added to titrated insulin therapy) reduced atherosclerosis, as measured by progression of common carotid artery intima-media thickness (cIMT), in adults with type 1 diabetes at increased risk for cardiovascular disease.

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1 This study explored the role of the potassium ion in endothelium-derived hyperpolarizing factor (EDHF)-mediated vasodilatation in the bovine coronary artery. 2 Bradykinin-induced, EDHF-mediated vasodilatation was blocked by the Na þ -K þ ATPase inhibitor, ouabain (1 mm), in a time-dependent manner, with maximal blockade seen after 90 min. In contrast, the K IR channel inhibitor, Ba 2 þ (30 mm), had no effect. 3 When the potassium content of the bathing solution was increased in a single step from 5.9 to 7 -19 mm, powerful vasodilatation (max. 75.973.6%) was observed. Vasodilatation was transient and, consequently, cumulative addition of potassium produced little vasodilatation, with vasoconstriction predominating at the higher concentrations. 4 The magnitude of potassium-induced vasodilatation was similar in endothelium-containing and endothelium-denuded rings, and was unaffected by Ba 2 þ (30 mm), but abolished by ouabain (1 mm). 5 Ouabain (1 mm, 90 min) powerfully blocked bradykinin-induced, nitric oxide-mediated vasodilatation as well as that induced by the nitrovasodilator, glyceryl trinitrate, but that induced by the K ATP channel opener, levcromakalim, was hardly affected. 6 Thus, activation of Na þ -K þ ATPase is likely to be involved in the vasodilator responses of the bovine coronary artery to both nitric oxide and EDHF. These findings, together with the ability of potassium to induce powerful, ouabain-but not Ba 2 þ -sensitive, endothelium-independent vasodilatation, are consistent with this ion contributing to the EDHF response in this tissue.

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