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• W2018672309 abstract "We have previously demonstrated that adenosine-mediated H 2 O 2 production and opening of ATP-sensitive K + (K ATP ) channels contributes to coronary reactive hyperemia. The present study aimed to investigate the roles of adenosine, H 2 O 2 , and K ATP channels in coronary metabolic hyperemia (MH). Experiments were conducted on isolated Langendorff-perfused mouse hearts using combined pharmacological approaches with adenosine receptor (AR) knockout mice. MH was induced by electrical pacing at graded frequencies. Coronary flow increased linearly from 14.4 ± 1.2 to 20.6 ± 1.2 ml·min −1 ·g −1 with an increase in heart rate from 400 to 650 beats/min in wild-type mice. Neither non-selective blockade of ARs by 8-( p-sulfophenyl)theophylline (8-SPT; 50 μM) nor selective A 2A AR blockade by SCH-58261 (1 μM) or deletion affected MH, although resting flow and left ventricular developed pressure were reduced. Combined A 2A AR and A 2B AR blockade or deletion showed similar effects as 8-SPT. Inhibition of nitric oxide synthesis by N-nitro-l-arginine methyl ester (100 μM) or combined 8-SPT administration failed to reduce MH, although resting flows were reduced (by ∼20%). However, glibenclamide (K ATP channel blocker, 5 μM) decreased not only resting flow (by ∼45%) and left ventricular developed pressure (by ∼36%) but also markedly reduced MH by ∼94%, resulting in cardiac contractile dysfunction. Scavenging of H 2 O 2 by catalase (2,500 U/min) also decreased resting flow (by ∼16%) and MH (by ∼24%) but to a lesser extent than glibenclamide. Our results suggest that while adenosine modulates coronary flow under both resting and ischemic conditions, it is not required for MH. However, H 2 O 2 and K ATP channels are important local control mechanisms responsible for both coronary ischemic and metabolic vasodilation." @default.
• W2018672309 created "2016-06-24" @default.
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• W2018672309 date "2014-10-01" @default.
• W2018672309 modified "2023-10-03" @default.
• W2018672309 title "Metabolic hyperemia requires ATP-sensitive K⁺ channels and H₂O₂ but not adenosine in isolated mouse hearts" @default.
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• W2018672309 doi "https://doi.org/10.1152/ajpheart.00421.2014" @default.
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