Pentolinium Tartrate - CAS 52-62-0
Catalog number: 52-62-0
Category: Inhibitor
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Molecular Formula:
C23H42N2O12
Molecular Weight:
538.59
COA:
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Targets:
nAChR
Description:
Pentolonium tartrate is the tartrate salt form of pentolinium, which is a ganglionic blocking agent and acts as a nicotinic acetylcholine receptor antagonist. It has been used as a ganglionic blocking agent in hypertension.
Purity:
98%
Appearance:
Solid powder
Synonyms:
1,1’-Pentamethylenebis(1-methylpyrrolidiniumtartrate);Ansolysenbitartrate;Tensilest tartrate;1-Methyl-1-[5-(1-methylpyrrolidin-1-ium-1-yl)pentyl]pyrrolidin-1-ium;(2R,3R)-2,3,4-trihydroxy-4-oxobutanoate
Solubility:
Soluble in DMSO, not in water
Storage:
2-8ºC
MSDS:
Inquire
Application:
Pentolonium tartrate has been used as a ganglionic blocking agent in hypertension.
Quality Standard:
In-house standard
Quantity:
Grams to Kilograms
Melting Point:
203 °C (decomp)
InChIKey:
HSMKTIKKPMTUQH-WBPXWQEISA-L
InChI:
InChI=1S/C15H32N2.2C4H6O6/c1-16(12-6-7-13-16)10-4-3-5-11-17(2)14-8-9-15-17;2*5-1(3(7)8)2(6)4(9)10/h3-15H2,1-2H3;2*1-2,5-6H,(H,7,8)(H,9,10)/q+2;;/p-2/t;2*1-,2-/m.11/s1
Canonical SMILES:
C[N+]1(CCCC1)CCCCC[N+]2(CCCC2)C.C(C(C(=O)[O-])O)(C(=O)O)O.C(C(C(=O)[O-])O)(C(=O)O)O
1.Role of sympathetic tone in BSO-induced hypertension in mice.
Rodríguez-Gómez I1, Baca Y, Moreno JM, Wangensteen R, Perez-Abud R, Payá JA, O'Valle F, Vargas F. Am J Hypertens. 2010 Aug;23(8):882-8. doi: 10.1038/ajh.2010.90. Epub 2010 Apr 29.
BACKGROUND: We investigated the contribution of the sympathetic tone to the hypertension induced by chronic administration of buthionine sulfoximine (BSO) and characterized this model in mice.
2.Cardiovascular responses to microinjection of noradrenaline into the medial amygdaloid nucleus of conscious rats result from α₂-receptor activation and vasopressin release.
Fortaleza EA1, Scopinho AA, Corrêa FM. Eur J Neurosci. 2011 May;33(9):1677-84. doi: 10.1111/j.1460-9568.2011.07655.x. Epub 2011 Mar 29.
The medial amygdaloid nucleus (MeA) is involved in the modulation of physiological and behavioral processes, as well as regulation of the autonomic nervous system. Moreover, MeA electrical stimulation evokes cardiovascular responses. Thus, as noradrenergic receptors are present in this structure, the present study tested the effects of local noradrenaline (NA) microinjection into the MeA on cardiovascular responses in conscious rats. Moreover, we describe the types of adrenoceptor involved and the peripheral mechanisms involved in the cardiovascular responses. Increasing doses of NA (3, 9, 27 or 45 nmol/100 nL) microinjected into the MeA of conscious rats caused dose-related pressor and bradycardic responses. The NA cardiovascular effects were abolished by local pretreatment of the MeA with 10 nmol/100 nL of the specific α₂-receptor antagonist RX821002, but were not affected by local pretreatment with 10 nmol/100 nL of the specific α₁-receptor antagonist WB4101.
3.The role of nitric oxide in the development of neurogenic pulmonary edema in spinal cord-injured rats: the effect of preventive interventions.
Sedy J1, Zicha J, Kunes J, Hejcl A, Syková E. Am J Physiol Regul Integr Comp Physiol. 2009 Oct;297(4):R1111-7. doi: 10.1152/ajpregu.00251.2009. Epub 2009 Aug 12.
Neurogenic pulmonary edema (NPE) is an acute life-threatening complication following an injury of the spinal cord or brain, which is associated with sympathetic hyperactivity. The role of nitric oxide (NO) in NPE development in rats subjected to balloon compression of the spinal cord has not yet been examined. We, therefore, pretreated Wistar rats with the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) either acutely (just before the injury) or chronically (for 4 wk prior to the injury). Acute (but not chronic) L-NAME administration enhanced NPE severity in rats anesthetized with 1.5% isoflurane, leading to the death of 83% of the animals within 10 min after injury. Pretreatment with either the ganglionic blocker pentolinium (to reduce blood pressure rise) or the muscarinic receptor blocker atropine (to lessen heart rate decrease) prevented or attenuated NPE development in these rats. We did not observe any therapeutic effects of atropine administered 2 min after spinal cord compression.
4.GABAA receptor dysfunction contributes to high blood pressure and exaggerated response to stress in Schlager genetically hypertensive mice.
Davern PJ1, Chowdhury S, Jackson KL, Nguyen-Huu TP, Head GA. J Hypertens. 2014 Feb;32(2):352-62. doi: 10.1097/HJH.0000000000000015.
OBJECTIVE: Schlager BPH/2J hypertensive mice have high blood pressure (BP) likely due to overactivity of the sympathetic nervous system regulated by neurons in amygdala-hypothalamic pathways. These areas are normally under tonic inhibition by GABA containing neurons that may be deficient in Schlager hypertensive mice as suggested by microarray analysis. In the present study, cardiovascular effects of chronic activation of GABAA receptors were examined in BPH/2J mice.
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Chemical Structure

CAS 52-62-0 Pentolinium Tartrate

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