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- W2063384255 abstract "We evaluated the function of Na + /K + ATPase and sarcolemmal K ATP channels in diabetic rat hearts. Six weeks after streptozotocin (STZ) injection, unidirectional K + fluxes were assayed by using 87 rubidium ( 87 Rb + ) MRS. The hearts were loaded with Rb + by perfusion with Krebs–Henseleit buffer, in which 50% of K + was substituted with Rb + . The rate constant of Rb + uptake via Na + /K + ATPase was reduced. K ATP -mediated Rb + efflux was activated metabolically with 2,4-dinitrophenol (DNP, 50 µmol·L –1 ) or pharmacologically with a K ATP channel opener, P-1075 (5 µmol·L –1 ). Cardiac energetics were monitored by using 31 P MRS and optical spectroscopy. DNP produced a smaller ATP decrease, yet similar Rb + efflux activation in STZ hearts. In K + -arrested hearts, P-1075 had no effect on high-energy phosphates and stimulated Rb + efflux by interaction with SUR2A subunit of K ATP channel; this stimulation was greater in STZ hearts. In normokalemic hearts, P-1075 caused cardiac arrest and ATP decline, and the stimulation of Rb + efflux was lower in normokalemic STZ hearts arrested by P-1075. Thus, the Rb + efflux stimulation in STZ hearts was altered depending on the mode of K ATP channel activation: pharmacologic stimulation (P-1075) was enhanced, whereas metabolic stimulation (DNP) was reduced. Both the basal concentration of phosphocreatine ([PCr]) and [PCr]/[ATP] were reduced; nevertheless, the STZ hearts were more or equally resistant to metabolic stress." @default.
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- W2063384255 date "2008-10-01" @default.
- W2063384255 modified "2023-09-24" @default.
- W2063384255 title "Potassium fluxes, energy metabolism, and oxygenation in intact diabetic rat hearts under normal and stress conditions" @default.
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- W2063384255 doi "https://doi.org/10.1139/y08-076" @default.
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