Levcromakalim inhibits spontaneous contractions completely in a glibenclamide-sensitive manner. LevCromakalim (5 μM) inhibits spontaneous contractions, which are recovered by glibenclamide. Levcromakalim (1, 5 and 10 μM) inhibits phasic contractions to 34±21.1%, 20.1±20.0% and 0% of the control. Glibenclamide reverses the inhibition of spontaneous isometric contractions caused by LevCromakalim (5 μM) to 84±1.5% of the control. Levcromakalim (20 and 100 μM) also inhibits oxytocin (OXT) (10 nM)-induced phasic contractions to 34±21.4% and 14±12.6% of the control [2]. LevCromakalim induces dose-dependent relaxation in both the young and old mesenteric artery (MAs); there is no difference in relaxation with age. However, the relaxation is markedly reduced in response to the high-salt (HS) diet in the old MAs (P<0.05). Maximum dilations to Levcromakalim (10-4 M) are 97 ± 3% in the young MAs versus 98 ± 1% in the young salt arteries, while dilations are 99±0.7% in the old MAs when compared with 85 ± 5% in the old salt arteries (P<0.05) [3].