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Role of Calcium-Activated Potassium Channels with Small Conductance in Bradykinin-Induced Vasodilation of Porcine Retinal Arterioles

¹From the Department of Pharmacology, Aarhus University, Aarhus C, Denmark; and the ²Department of Ophthalmology, Aarhus University Hospital, Aarhus C, Denmark.

PURPOSE. Endothelial dysfunction and impaired vasodilation may be involved in the pathogenesis of retinal vascular diseases. In the present study, the mechanisms underlying bradykinin vasodilation were examined and whether calcium-activated potassium channels of small (SK_Ca) and intermediate (IK_Ca) conductance are involved in regulation of endothelium-dependent vasodilation in retinal arterioles was investigated.

METHODS. Porcine retinal arterioles (diameter 112 µm, N = 119) were mounted in microvascular myographs for isometric tension recordings. The arterioles were contracted with the thromboxane analogue, U46619, and concentration–response curves were constructed for bradykinin and a novel opener of SK_Ca and IK_Ca channels, NS309.

RESULTS. In U46619-contracted arterioles, bradykinin and NS309 induced concentration-dependent relaxations. In vessels without endothelium, bradykinin relaxation was abolished and NS309 relaxation was attenuated. Inhibition of NO synthase with asymmetric dimethylarginine and/or cyclooxygenase with indomethacin markedly reduced bradykinin and NS309 relaxation. NO synthase and cyclooxygenase inhibition together with oxyhemoglobin abolished bradykinin relaxation and attenuated NS309 relaxation. Blocking of SK_Ca and IK_Ca channels with apamin plus charybdotoxin or blocking of SK_Ca channels alone in the absence and the presence of indomethacin markedly reduced bradykinin and NS309 relaxation, whereas blocking of IK_Ca channels had no significant effect. In vessels without endothelium, blocking of SK_Ca channels alone had no effect on sodium nitroprusside-induced relaxation.

CONCLUSIONS. In porcine retinal arterioles, NO and prostaglandins mediate endothelium-dependent relaxation to bradykinin and NS309. Moreover, these findings suggest that SK_Ca channels contribute to NO-mediated relaxation induced by bradykinin and NS309 and, hence, may play an important role in retinal arterial endothelial function.

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