Disease relevance of Dimethylphenylpiperazinium

• K+-evoked release was unaffected by hypoxia (PO2 approximately 30-38 mm Hg), but release evoked by DMPP was significantly increased [1].
• Another result of the research was the identification of DMPP analogues, such as 3a (K(i) = 90 nM) and 14b (K(i) = 180 nM), that maintain affinity for the central nicotinic receptor when the ammonium function is changed into an aminic one and are therefore possible leads for drug development in neurodegenerative diseases [2].
• The uptake of Ca++ by ganglion cells is not an adequate stimulus for cGMP accumulation because the nicotinic receptor agonist dimethylphenylpiperazinium increases 45Ca-uptake but has no effect on cGMP formation in ganglia [3].
• 4. The four omega-conotoxins as well as atropine produced similar partial inhibition (53-62%) of the contractures evoked by dimethylphenylpiperazinium, while tetrodotoxin inhibited the contracture completely [4].
• When tachycardia was induced by chemical stimulation of nicotinic (DMPP), muscarinic (McN-A-343-11) or histamine receptors in the stellate ganglia, opiates were still active in reducing the effect of these chemicals [5].

High impact information on Dimethylphenylpiperazinium

• Neuropeptide Y also blocked nerve-mediated phasic contractions of the circular muscle, induced by dimethylphenylpiperazinium or ceruletide, and abolished the peristaltic movements of the small intestine [6].
• Since muscarinic cholinergic agonists cause inhibition of somatostatin secretion, the observed net increase in somatostatin suggests that 1,1 dimethyl-4-phenylpiperazinium activated predominantly a noncholinergic stimulatory neuron [7].
• From this it was concluded that 1,1-dimethyl-4-phenylpiperazinium activates intramural cholinergic and noncholinergic neurons to cause gastrin secretion, 1,1-dimethyl-4-phenylpiperazinium also caused a biphasic, dose-dependent increase in somatostatin secretion [7].
• Both assays provided the same rank orders of potency for (+/-)-epibatidine, 2S-(-)-nicotine, 7R,9S-(-)-cytisine, and 1,1-dimethyl-4-phenylpiperazinium in a cell line expressing rat alpha 3 beta 4 receptors [8].
• Addition of guinea pig brain synaptosomal incubation medium or whole brain extracts to assays in which 1,1-dimethyl-4-phenylpiperazinium-evoked release of [3H]AcCho from guinea pig myenteric plexus synaptosomes reversed purinergic, muscarinic, and alpha 2-adrenergic agonist inhibition [9].

Chemical compound and disease context of Dimethylphenylpiperazinium

• We have used the human sympathetic neuronal line SH-SY5Y to investigate the effects of hypoxia on noradrenaline (NA) release evoked by either raised [K+]o (100 mM) or the nicotinic acetylcholine receptor (nAChR) agonist dimethylphenylpiperazinium iodide (DMPP) [1].
• The ganglion stimulant drug dimethylphenylpiperazinium (32 microM) also stimulated the release of substance P; its effect was completely prevented by hexamethonium (240 microM) [10].
• ICS 205-930 was selective in its action since it had no effect on dimethylphenylpiperazinium (DMPP) responses in either ganglion or on GABA responses in NG [11].
• 3. Agmatine (10 mM) substantially blocks both DMPP-induced depolarizations of rat superior cervical ganglion and synaptic transmission through the ganglion [12].
• After pretreatment with atropine (0.2 mg/kg), an intravenous bolus (4 microg/kg) of a nicotinic ganglion stimulant [1,1-dimethyl-4-phenylpiperazinium iodide (DMPP)] was given at rest and during treadmill exercise at graded intensities [13].

Biological context of Dimethylphenylpiperazinium

• Activation of DMPP-sensitive nAChRs during the second larval stage uncouples a molting timer and a developmental timer, thus causing a heterochronic phenotype that is lethal at the subsequent molt [14].
• In intact cells, 1,1-dimethyl-4-phenylpiperazinium (DMPP) induced Ca2+-dependent phosphorylation of at least 17 proteins which were detected by two-dimensional gel electrophoresis [15].
• Overexpression of either chromaffin cell or brain Rabphilin3a by transfection with the corresponding cDNAs in mammalian expression vectors enhanced DMPP-induced secretion of co-expressed human growth hormone (GH) approximately 30% [16].
• A similar IC50 (approximately 18 microM) for inhibition of both DMPP- and veratridine-stimulated Na+ uptake was obtained [17].
• Under current-clamp conditions, pressure ejections of DMPP depolarized cells and induced the discharge of action potentials [18].

Anatomical context of Dimethylphenylpiperazinium

• The mixed nicotinic-muscarinic agonist carbachol and the nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium, but not the muscarinic agonist muscarine, caused 3-10% of the total protein kinase C activity to become membrane-bound within 3 min in intact chromaffin cells [19].
• The affinities of alpha3beta2 receptors expressed in oocytes were similar to the affinities of native alpha3 containing receptors from SH-SY5Y cells for acetylcholine, cytisine, and 1,1-dimethyl-4-phenylpiperazinium [20].
• LOS smooth muscle responses were recorded in response to electrical field stimulation (EFS), potassium chloride (KCl), DMPP, isoprenaline, capsaicin, bethanechol, and tachykinins [21].
• Stimulation of the pelvic ganglia by an application of dimethylphenylpiperazinium contracted the distal colon [22].
• Prejunctional effects of the nicotinic ACh receptor agonist dimethylphenylpiperazinium at the rat neuromuscular junction [23].

Associations of Dimethylphenylpiperazinium with other chemical compounds

• The gastrin response was abolished by hexamethonium but only partly inhibited (35% at the higher dose of 1,1-dimethyl-4-phenylpiperazinium) by atropine [7].
• If the osmolality of the external medium is made either hyper- or hypoosmotic, 1,1-dimethyl-4-phenylpiperazinium iodide-induced release of endogenous catecholamines is inhibited [24].
• Current responses evoked by rapid application of cholinergic agonists (acetylcholine, nicotine, or 1,1-dimethyl-4-phenylpiperazinium) were recorded from voltage-clamped oocytes [25].
• Chromaffin cell catecholamine secretion was stimulated by either boluses of potassium (K+) or the nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium (DMPP) [26].
• Effects on serotonin of (-)nicotine and dimethylphenylpiperazinium in the dorsal raphe and nucleus accumbens of freely behaving rats [27].

Gene context of Dimethylphenylpiperazinium

• 1,1-Dimethyl-4-phenylpiperazinium (DMPP) (10(-5) and 10(-4) M) and bombesin-14 (10(-8) and 10(-6) M) caused concentration-dependent increases in somatostatin secretion that were of the same magnitude in antral and fundic segments [28].
• 1,1-Dimethyl-4-phenylpiperazinium (10(-5) to 10(-4) M) caused a biphasic dose-dependent increase in gastrin secretion [7].
• The PI3K inhibitors wortmannin and LY294002 abrogated the inhibitory effect of DMPP on LPS-induced TNF release by monocytes [29].
• The effect of vasoactive intestinal polypeptide (VIP) receptor antagonism on preganglionic vagal electrical stimulation and on vagal postganglionic activation using nicotine and 1,1-dimethyl-4-phenylpiperazinium iodide on cardiac interval was evaluated in the isolated innervated rat right atrium [30].
• To examine the role of TNF-alpha as a modulator of autonomic function of the PNS, we measured [3H]norepinephrine ([3H]NE) secretion evoked by 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP), a nicotinic agonist, in cultures from neonatal rat superior cervical ganglia (SCG) [31].

Analytical, diagnostic and therapeutic context of Dimethylphenylpiperazinium

• Perfusion with DMPP (10(-6) to 10(-3) M) caused a rapid, transient elevation in [Ca++]i which was abolished by Ca(++)-free medium containing 1 mM EGTA.(ABSTRACT TRUNCATED AT 250 WORDS)[32]
• Longitudinal muscle contractions caused by the nAChRs agonists, dimethylphenylpiperazinium (DMPP), nicotine, and cytisine were measured using isometric strain gauge transducers [33].
• It is concluded that the inhibitory muscarinic mechanism modulates similarly the ACh release evoked by DMPP or high potassium and the release caused by electrical stimulation [34].
• In addition, the effects of DMPP on CP were abolished by bilateral adrenal demedullation, but were unaltered by hindlimb denervation [35].
• In dogs in which the coeliac and superior mesenteric ganglia had previously been removed, MNS caused no response although intra-arterial injection of 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP, 0.1 mumol) caused marked contractions [36].

References