Streptozotocin-diabetes alters action potentials in rat diaphragm.
This study tested the hypothesis that diabetes alters diaphragm action potentials and electrophysiological responses to K(+) channel blockade. Intracellular recordings were performed in vitro in diaphragm fibers from streptozotocin-induced diabetic and normal Wistar rats (glucose 670+/-31 vs. 252+/-14 mg/dl). Comparing diabetic to normal muscle properties, resting membrane potential was significantly depolarized (-72.2+/-0.8 vs. -77.4+/-1.1 mV), action potential 50% repolarization time was significantly accelerated (0.33+/-0.01 vs. 0.39 +/-0.01 msec), and action potential area was significantly decreased (59.4+/-2.3 vs. 70.7+/-2.2 mV msec). The K(+) channel blocker 3,4-diaminopyridine (DAP) depolarized resting membrane potential of normal but not diabetic muscle. DAP significantly prolonged action potential repolarization and significantly increased action potential area, but significantly more in normal than diabetic muscle. These data indicate that diabetes shortens diaphragm action potentials, which appears to be due to altered K(+) channels.[1]References
- Streptozotocin-diabetes alters action potentials in rat diaphragm. van Lunteren, E., Moyer, M. Respiratory physiology & neurobiology. (2003) [Pubmed]
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