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Inhibition of NO synthase with L-Name produced a modest increase the coronary blood flow response to intracoronary NaHS (n=3) (A). Coronary vasodilation to NaHS was unaffected by the inhibition of voltage-dependent K+ channels with 4-AP (n=3) while blockade of KATP channels with glibenclamide (n=5) markedly reduced NaHS-induced dilation in the coronary circulation. # P < 0.05; * P < 0.001.
