Endothelium is involved in the vasorelaxation by an ATP-sensitive K+ channel opener, NIP-121

Tanaka, Yoshio; Yamaki, Fumiko; Hirano, Haruko; Otsuka, Akiko; Tanaka, Hikaru; Shigenobu, Koki

doi:10.1016/s0014-2999(98)00960-1

Cited by 2 publications

(1 citation statement)

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“…In the rat mesenteric arterial bed, removal of basal NO significantly augmented the responses to KCOs via cyclic GMP dependent mechanisms (McCulloch & Randall, 1996). On the other hand, the vasorelaxing effect of a KCO in endothelium‐intact rat aorta was more potent than in an endothelium‐denuded one (Tanaka et al ., 1999). The amount of NO released from endothelium in small arterioles is substantially greater than that in large arteries, possibly being involved in the difference of effects of NO on vasorelaxation to KCOs.…”

Section: Discussionmentioning

confidence: 99%

Levcromakalim causes indirect endothelial hyperpolarization via a myo‐endothelial pathway

Murai

Muraki

Imaizumi

et al. 1999

British J Pharmacology

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1 E ects of K + channel opener, levcromakalim, on vascular endothelial cells were examined. Under voltage-and current-clamp conditions, application of acetylcholine to dispersed endothelial cells isolated from rabbit superior mesenteric artery (dispersed RMAECs) produced hyperpolarization and outward currents. On the other hand, dispersed RMAECs did not respond to levcromakalim. 2 When membrane potential was recorded from endothelium in a mesenteric arterial segment, exposure to levcromakalim in a concentration range of 0.1 to 3 mM caused concentration-dependent hyperpolarization. The hyperpolarization was observed in the absence of external Ca 2+ and was inhibited by 10 mM glibenclamide. 3 The presence of 1 mM heptanol did not a ect the levcromakalin-induced hyperpolarization, whereas treatment of the mesenteric arterial segment with 20 mM 18 b-glycyrrhetinic acid signi®cantly reduced the hyperpolarization. The response to acetylcholine of RMAECs in an arterial segment with 18 b-glycyrrhetinic acid was, however, similar to that without 18 bglycyrrhetinic acid. 4 These suggest that although RMAECs themselves are functionally insensitive to levcromakalim, those in an arterial segment are hyperpolarized by levcromakalim via myo-endothelial electrical communication.

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Section: Discussionmentioning

confidence: 99%