Acetylcholine

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Lee A Dawson - One of the best experts on this subject based on the ideXlab platform.

Marie L Woolley - One of the best experts on this subject based on the ideXlab platform.

Masato Tsutsui - One of the best experts on this subject based on the ideXlab platform.

  • ikarisoside a inhibits Acetylcholine induced catecholamine secretion and synthesis by suppressing nicotinic Acetylcholine receptor ion channels in cultured bovine adrenal medullary cells
    Naunyn-schmiedebergs Archives of Pharmacology, 2015
    Co-Authors: Xiaojia Li, Takafumi Horisita, Noriaki Satoh, Yukari Yoshinaga, Susumu Ueno, Yumiko Toyohira, Munekazu Iinuma, Keita Takahashi, Han Zhang, Masato Tsutsui
    Abstract:

    Ikarisoside A is a natural flavonol glycoside derived from plants of the genus Epimedium, which have been used in Traditional Chinese Medicine as tonics, antirheumatics, and aphrodisiacs. Here, we report the effects of ikarisoside A and three other flavonol glycosides on catecholamine secretion and synthesis in cultured bovine adrenal medullary cells. We found that ikarisoside A (1–100 μM), but not icariin, epimedin C, or epimedoside A, concentration-dependently inhibited the secretion of catecholamines induced by Acetylcholine, a physiological secretagogue and agonist of nicotinic Acetylcholine receptors. Ikarisoside A had little effect on catecholamine secretion induced by veratridine and 56 mM K+. Ikarisoside A (1–100 μM) also inhibited 22Na+ influx and 45Ca2+ influx induced by Acetylcholine in a concentration-dependent manner similar to that of catecholamine secretion. In Xenopus oocytes expressing α3β4 nicotinic Acetylcholine receptors, ikarisoside A (0.1–100 μM) directly inhibited the current evoked by Acetylcholine. It also suppressed 14C-catecholamine synthesis and tyrosine hydroxylase activity induced by Acetylcholine at 1–100 μM and 10–100 μM, respectively. The present findings suggest that ikarisoside A inhibits Acetylcholine-induced catecholamine secretion and synthesis by suppression of nicotinic Acetylcholine receptor-ion channels in bovine adrenal medullary cells.

F. Schlemmer - One of the best experts on this subject based on the ideXlab platform.

  • Differential effects of calcium channel antagonists (ω-conotoxin GVIA, nifedipine, verapamil) on the electrically-evoked release of [^3H]Acetylcholine from the myenteric plexus, phrenic nerve and neocortex of rats
    Naunyn-Schmiedeberg's Archives of Pharmacology, 1990
    Co-Authors: I. Wessler, D. J. Dooley, J. Werhand, F. Schlemmer
    Abstract:

    Electrically-evoked release of [^3H]Acetylcholine from autonomic neurons (myenteric plexus), motoneurons (phrenic nerve) and the central nevous system (neocortex) was investigated in the presence and absence of the calcium channel antagonists ω-conotoxin GVIA, nifedipine and verapamil, whereby the same species (rat) was used in all experiments. Release of [^3H]Acetylcholine was measured after incubation of the tissue with [^3H]choline. ω-Conotoxin GVIA markedly reduced (70%) the evoked release of [^3H]Acetylcholine from the myenteric plexus of the small intestine (IC_50: 0.7 nmol/l) with a similar potency at 3 and 10 Hz stimulation. An increase in the extracellular calcium concentration attenuated the inhibitory effect of ω-conotoxin GVIA. Release of [^3H]Acetylcholine from the rat neocortex was also inhibited (90%) by ω-conotoxin GVIA, but the potency was 19-fold lower (IC_50: 13 nmol/l). However, the release of [^3H]Acetylcholine from the phrenic nerve was not reduced by ω-conotoxin GVIA (100 nmol/l) at 1.8 mmol/l calcium (normal concentration), whereas ω-conotoxin GVIA inhibited evoked [^3H]Acetylcholine release by 47% at 0.9 mmol/l calcium. Neither nifedipine (0.1 and 1 μmol/l) nor verapamil (0.1, 1 and 10 μmol/l) modified the evoked release of [3H]Acetylcholine from the myenteric plexus and the phrenic nerve. Acetylcholine release from different neurons appears to be regulated by different types of calcium channels. N-type channels play the dominant role in regulating Acetylcholine release from both the myenteric plexus and the neocortex, whereas Acetylcholine release from motor nerves is regulated by calcium channel(s) not yet characterized.

C J Garland - One of the best experts on this subject based on the ideXlab platform.

  • differential effects of Acetylcholine nitric oxide and levcromakalim on smooth muscle membrane potential and tone in the rabbit basilar artery
    British Journal of Pharmacology, 1993
    Co-Authors: Trances Plane, C J Garland
    Abstract:

    1 Endothelium-dependent hyperpolarization of smooth muscle cells in isolated, pre-contracted segments of rabbit basilar artery in response to acetycholine (100 μm) was abolished in the presence of glibenclamide (10 μm). 2 Acetylcholine-evoked relaxation was unaffected by either glibenclamide or 65 mm potassium chloride, indicating that the change in membrane potential did not form an essential component of relaxation and that high concentrations of potassium did not inhibit the release or action of endothelium-derived relaxing factor in this vessel. 3 Saturated solutions of nitric oxide (NO) gas in solution (150 μm), which evoked maximal relaxation of arterial segments pre-contracted and depolarized by noradrenaline (10–100 μm), did not alter the membrane potential of either unstimulated or depolarized smooth muscle cells. 4 The potassium channel opener levcromakalim, evoked concentration-dependent relaxation and hyperpolarization in pre-constricted smooth muscle cells. The threshold concentrations for hyperpolarization and relaxation, the EC50 values and the maximally effective concentration of levcromakalim (around 30 nm, 150 nm and 10 μm, respectively) were not significantly different, and both components of the response were inhibited by glibenclamide (10 μm), indicating a close coupling between the two responses. 5 In the presence of 65 mm potassium chloride, the hyperpolarization to levcromakalim was abolished, while a small relaxation (25 ± 4%) persisted, indicating an additional mechanism for relaxation to this agent. 6 These results show that different mechanisms underlie the relaxant action of potassium channel openers, NO and endothelium-derived factors in cerebral arteries and provide further evidence that in the basilar artery, in contrast to some other vessels, endothelium-dependent hyperpolarization to Acetylcholine is not important for smooth muscle relaxation.