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. 2015 May 20;3(3):e00150. doi: 10.1002/prp2.150

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© 2015 The Authors. Pharmacology Research & Perspectives published by John Wiley & Sons Ltd, British Pharmacological Society and American Society for Pharmacology and Experimental Therapeutics.

This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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The mechanism underlying the impairment of endothelium-dependent hyperpolarization (EDH)-type relaxations in aging or hypertensive rats. Aging or hypertension causes the dysfunction of small-conductance calcium-activated potassium chanels (SK_C_a) and sodium-potassium ATPase (Na-K ATPase), thus impairing EDH-mediated responses. In young hypertensive animals, the impairment is compensated by the facilitation of the activity of intermediate-conductance calcium-activated potassium chanels (IK_C_a), and the activation of adenosine monophosphate-activated protein kinase (AMPK) and silent information regulator T1 (sirtuin-1; SIRT1).