Key result
Glimepiride potently blocks pinacidil-activated cardiac K(ATP) channels (IC50 6.8 nM) but is much less effective when channels are activated by metabolic inhibition.
Effect estimate: IC50 6.8 nM
Glimepiride potently blocks cardiac K(ATP) channels, but its blocking efficacy is significantly reduced during metabolic inhibition, possibly due to increased intracellular ADP.
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Glimepiride K(ATP) blockade weakens during metabolic inhibition; leaves open whether this alters sulfonylurea effects in cardiac ischemia.
Lawrence et al. (2002) studied this question. Glimepiride vs. Glibenclamide / unblocked state was evaluated on Blockade of K(ATP) currents (IC50 6.8 nM). Glimepiride potently blocks pinacidil-activated cardiac K(ATP) channels (IC50 6.8 nM) but is much less effective when channels are activated by metabolic inhibition.
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