(±)-Vesamicol hydrochloride - CAS 120447-62-3
Category: Inhibitor
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Molecular Formula:
Molecular Weight:
(±)-Vesamicol hydrochloride is an inhibitor of acetylcholine transport (Ki = 2 nM) that blocks the loading of acetylcholine into synaptic vesicles of cholinergic nerve terminals. The inhibition by Vesamicol attenuates acetylcholine neuronal signaling without direct effecys on signaling mechanisms.
Brife Description:
acetylcholine transport inhibitor
≥99% by HPLC
Related CAS:
22232-64-0 (free base)
(±)-trans-2-(4-Phenylpiperidinyl)cyclohexanol hydrochloride; AH 5183 hydrochloride; AH-5183 hydrochloride; 2-(4-Phenylpiperidino)cyclohexanol hydrochloride; Cyclohexanol, 2-(4-phenylpiperidino)-, hydrochloride
Canonical SMILES:
1.Cardiac rehabilitation/exercise in patients with implantable cardioverter defibrillators.
Friedman AW;Lipman RC;Silver SJ;Minella RA;Hoover JL J Natl Med Assoc. 1996 Jun;88(6):374-8.
There have been no specific exercise or daily activity guidelines determined for patients with automatic implantable cardioverter defibrillators. Two patients, one with a Ventritex Cadence Model V-100 defibrillator and one with a CPI Ventak Model 1550 defibrillator were enrolled in monitored cardiac rehabilitation. One patient had symptoms of syncope and cardiodefibrillation during a vigorous short walk prior to cardiac rehabilitation and became fearful of any activity. Stress testing on this patient was terminated early because his atrial fibrillation rate approached the defibrillization rate. A low dose of beta blockade was added to his regimen. He underwent repeat stress testing and was placed in cardiac rehabilitation. This patient had no further shocks, and it was assumed that his shock was due to high atrial fibrillation rates. The second patient experienced recurrent shocks on amiodarone, propafenone, and mexiletine with presyncope. However, stress testing did not disclose abnormalities. The patient was fearful of any activity and was placed in cardiac rehabilitation. During an average of 26 sessions of cardiac rehabilitation, no symptoms have been noted, and the patients have returned to a more normal lifestyle.
2.[Insulin pumps and drop in pressure].
Aanderud L;Hansen EM Tidsskr Nor Laegeforen. 1994 Feb 20;114(5):570-2.
Do insulin pumps deliver more insulin at lower environmental pressures and, if so, is this due to pump dysfunction or to formation of bubbles in the insulin solutions? H-TRON V-100 (Hoechst Infusor V-100), MRS-1 (Disetronic), Nordic Infusor MK II (Novo Nordisk) and Minimed 504-S (Minimed Technology) insulin pumps were studied at 0.9 ATA and 0.8 ATA with constant infusion 2.0 I.U./hour. H-TRON V-100 was also studied at 0.7 ATA at the same infusion rate and with the motor in stop position. The results indicated that all pumps delivered slightly more insulin than the set rate during decompression (max. single value 2.68 I.U. extra delivered at 0.7 ATA, max. average value 1.32 I.U. extra delivered at 0.8 ATA). An equivalent amount of insulin (1.72 I.U.) was delivered at 0.7 ATA without running the motor. This implies that the extra insulin supplied was caused by physically dissolved nitrogen and oxygen in the insulin solution, and was not due to dysfunction of the pumps.
3.The nature and origin of calcium-insensitive miniature end-plate potentials at rodent neuromuscular junctions.
Lupa MT;Tabti N;Thesleff S;Vyskocil F;Yu SP J Physiol. 1986 Dec;381:607-18.
1. To study the nature and origin of slow-rising, Ca2+-insensitive miniature end-plate potentials (m.e.p.p.s) in mammalian muscle we used intracellular recording techniques and drugs which block acetylcholine (ACh) synthesis or the uptake of ACh into synaptic vesicles. Slow m.e.p.p.s were induced in vivo by paralysing the extensor digitorum longus muscle of the rat with botulinum toxin type A or in vitro by the application of 4-aminoquinoline to the mouse diaphragm nerve-muscle preparation. 2. Hemicholinium-3, which blocks ACh synthesis, reduced the amplitude of all synaptic potentials including slow m.e.p.p.s, but only if the nerve was stimulated. 3. 2(4-phenylpiperidino)cyclohexanol (AH-5183), which blocks the active uptake of ACh into synaptic vesicles, reduced both the frequency and the amplitude of slow m.e.p.p.s and did so without requiring nerve stimulation. 4. No correlation was observed between the molecular leakage of ACh from the motor nerve and the frequency and amplitude of slow m.e.p.p.s. 5. We conclude that slow m.e.p.p.s are caused by the release of ACh from the nerve terminal, possibly from a small pool of synaptic vesicle-like structures.
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CAS 120447-62-3 (±)-Vesamicol hydrochloride

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