Key result
P-1075 and 2,4-dintrophenol activated Rb(+) efflux from mouse hearts by approximately 35% compared to baseline conditions.
Demonstrates the feasibility of using 87Rb MRS to measure potassium transport kinetics in isolated mouse hearts, providing a baseline for future transgenic studies.
Validates 87Rb MRS for K+ transport in isolated mouse hearts; leaves open translation to transgenic models and clinical use.
We studied the fluxes of a potassium congener (Rb(+)) in mouse hearts by (87)Rb MRS at 8.4T. The hearts were loaded with Rb(+) by perfusion with Krebs-Henseleit buffer, in which 50% of K(+) was substituted with Rb(+). We initiated Rb(+) efflux by changing the perfusion medium to Rb(+)-free buffer. Spectra were acquired every 1.85 min, and the kinetics of Rb(+) transport were analyzed by means of monoexponential fits. The rate constants of Rb(+) uptake and efflux were 0.0680 +/- 0.0028 and 0.0510 +/- 0.0051 min(-1), respectively (approximately 30% faster than in the rat heart). The ATP-sensitive potassium channel opener, P-1075 (5 microM), and mitochondrial uncoupler, 2,4-dintrophenol (50 microM), activated Rb(+) efflux from mouse hearts by approximately 35%. The mechanisms responsible for the differences in Rb(+) uptake and efflux under baseline conditions and stimulation, in comparison with rat hearts, are discussed. These data provide a background for studies of cardiac potassium transport in transgenic mouse strains.
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Jilkina et al. (2005) studied Mouse hearts (animal model). P-1075 and 2,4-dintrophenol vs. Baseline conditions was evaluated on Rb(+) uptake and efflux rate constants. P-1075 and 2,4-dintrophenol activated Rb(+) efflux from mouse hearts by approximately 35% compared to baseline conditions.
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