Disease relevance of Hexamethonium chloride

• Pharmacological analysis revealed that the effects of 13-Nle-M on the gastrointestinal muscle are not mediated via nervous pathways: ganglion blockade by hexamethonium, blockade of axonal conduction by tetrodotoxin, or anticholinergic action by atropine failed to affect 13-Nle-M actions [1].
• Treatment with hexamethonium before smoking reversed the effect of the smoke on the colitis, improving all parameters [2].
• Cholinergic innervation in the aganglionic bowel of the piebald lethal mouse model of Hirschsprung's disease was investigated by analysis of muscarinic acetylcholine receptors before and after administration of hexamethonium [3].
• In the recovery period, the control dogs and the hexamethonium-treated dogs showed gradual increases in total peripheral resistance and in vasoconstricted hypertension 3 hours after stopping the infusion [4].
• Deficiency of alpha5 subunits strikingly increased the sensitivity to a low concentration of hexamethonium, leading to a nearly complete blockade of bradycardia in response to vagal stimulation [5].

Psychiatry related information on Hexamethonium chloride

• Hexamethonium slightly decreased the percent correct responses, while not interfering with motor activity of rats [6].
• Amnesia induced by stimulation of the amygdala is attenuated by hexamethonium [7].
• Further, mecamylamine restored the nicotine-induced disruption of individual differences; hexamethonium had no effect [8].
• To investigate the effects of chronic nicotine administration on feeding behavior, hexamethonium, a nicotinic blocker with mainly peripheral actions, was acutely given to rats during and after chronic nicotine administration [9].

High impact information on Hexamethonium chloride

• Decamethonium and hexamethonium block K+ channels of sarcoplasmic reticulum [10].
• Also, the Cl- secretion, but not the increase in prostaglandin production, was reduced by enteric nervous system blockade with tetrodotoxin, hexamethonium, or atropine [11].
• In the presence of hexamethonium, vagal stimulation failed to affect insulin, glucagon, or somatostatin secretion [12].
• Increases in left ventricular systolic pressure and maximum derivative of pressure with respect to time (dP/dtmax) resulting from electrical stimulation of preganglionic sympathetic nerves were not significantly altered by lidocaine, but were markedly attenuated by hexamethonium, a ganglionic blocker [13].
• The effect of OP-CCK on the gallbladder was partially blocked by tetrodotoxin (P < 0.02), hexamethonium alone (P < 0.05), or a combination of hexamethonium and atropine (P < 0.01) [14].

Chemical compound and disease context of Hexamethonium chloride

• NG-Nitro-L-arginine-induced hypertension was markedly attenuated or abolished by treatment with hexamethonium; this inhibition was still observed when the blood pressure fall caused by the ganglionic blocking agent was compensated by continuous infusion of angiotensin II [15].
• The degree of protection against inhaled histamine achieved by inhalation of the ganglion blocker hexamethonium bromide plus placebo, hexamethonium plus atropine sulphate, and placebo plus placebo was examined in six atopic subjects, four of whom had current asthma [16].
• The acute hypertension was also associated with increased neurogenic vasoconstrictor tone since hexamethonium markedly reduced MAP, MR, HQR and non-stenotic RR [17].
• 4. The reflex response to carotid body chemoreceptor stimulation, by hypoxia, was not altered by hexamethonium bromide but was greatly reduced by the hyoscine methyl bromide [18].
• Decanoic acid induced motor activity was reversibly abolished by tetrodotoxin (3 microm), hyoscine (1 microm) and hexamethonium (100 microm), but was insensitive to blockade of P2 purinoceptors by PPADS (60 microm) [19].

Biological context of Hexamethonium chloride

• Infusion of phentolamine (0.25 mg/min) into the renal artery, intravenous hexamethonium (l mg/kg), adrenal demedullation, or cooling the cervical vagi prevented postarrhythmic renal vasoconstriction [20].
• Blockade of muscarinic or nicotinic receptors by hyoscine or hexamethonium decelerated peristalsis up to propulsion arrest [21].
• In addition, postoperative neural blockade with hexamethonium (1 mg/kg intraperitoneally) or guanethidine (50 mg/kg intraperitoneally) normalized gastric emptying without affecting small-intestinal transit [22].
• The inotropic response was similar despite reflex blockade with hexamethonium or volume reexpansion, indicating its independence from baroreflex stimulation [23].
• The action of nicotine was insensitive to alpha-bungarotoxin and to neuronal bungarotoxin, but was blocked by mecamylamine, hexamethonium, curare, and DHBE, with IC50 values different from those reported for IPN postsynaptic nAChRs [24].

Anatomical context of Hexamethonium chloride

• To determine whether a synaptic link with nicotinic transmission was present, we investigated the effect of hexamethonium on vagal-stimulated lower esophageal sphincter relaxation [25].
• Hexamethonium (100 micromol/L) inhibited fEPSPs in the gastric corpus by 98% +/- 1% (n = 31) and in the duodenum, ileum, taenia coli, proximal colon, and distal colon by 42%-55% [26].
• RESULTS: Prior close-intra-arterial infusions of tetrodotoxin or hexamethonium had no significant effect on the contractile response to any agonist, indicating that they acted primarily on smooth muscle muscarinic receptors [27].
• Conclusions: The vagus nerve plays a counterinflammatory role in acute colitis via a macrophage-dependent mechanism, involving hexamethonium-sensitive nicotinic receptors [28].
• This effect is reversed by hexamethonium, suggesting that a neural pathway is involved [2].

Associations of Hexamethonium chloride with other chemical compounds

• Tetrodotoxin and hexamethonium reduced the release of 5-HT by 30%-40% in a nonadditive manner, indicating a spontaneous neuronal (nicotinic) excitatory input to the enterochromaffin cells [29].
• Tetrodotoxin, phentolamine, hexamethonium, methysergide, and bilateral cervical vagotomy did not alter the response of the LES to substance P [30].
• The LES response to motilin was abolished by hexamethonium and significantly antagonized by atropine and 4-diphenylacetoxy-N-methylpiperidine methiodide, but was not affected by pirenzepine, phentolamine, or naloxone [31].
• The contraction generated by synthetic canine motilin (10(-5) M) was not influenced by atropine, hexamethonium, tetrodotoxin, naloxone, or sodium nitroprusside (all used at 10(-4) M) but was blocked by verapamil (10(-4)) [32].
• These responses were inhibited totally or mostly by capsaicin, administered neonatally, topically, or perineurally, by topical lidocaine, and by parenteral administration of substance P antiserum, somatostatin, or hexamethonium [33].

Gene context of Hexamethonium chloride

• 2. In anaesthetized rats pretreated with hexamethonium, infusion of ET-1 (10(-11) mol kg-1 min-1) increased the mean arterial pressure (MAP) from 93 +/- 1.5 mmHg to 137 +/- 2.4 mmHg after 70 min (n = 29) [34].
• Veratridine-stimulated short-circuit current (I(sc)) responses in +/+, Y(1) or Y(2) antagonist pretreated +/+ colon, Y(1)-/- and NPY-/- colon were insensitive to cholinergic blockade by atropine (At; 1 microM) and hexamethonium (Hex; 10 microM) [35].
• The CGRP-induced relaxations were unaffected by hexamethonium and partly reduced (about 40%) by tetrodotoxin [36].
• The effects of lumbosacral oxytocin were partly mimicked by the oxytocin agonist [Thr(4),Gly(7)]-oxytocin blocked by the oxytocin receptor antagonist atosiban and by hexamethonium [37].
• The stimulatory effect of peripherally administered CRF on colonic motility was abolished by truncal vagotomy, hexamethonium, atropine, and intracisternal injection of astressin (a CRF receptor antagonist) [38].

Analytical, diagnostic and therapeutic context of Hexamethonium chloride

• Truncal vagotomy and administration of hexamethonium significantly reduced nonadrenergic, noncholinergic relaxation, the catalytic activity of NOS, the number of NOS-immunoreactive cells, and the density of NOS-immunoreactive bands and NOS mRNA bands obtained from gastric tissue [39].
• The effects of the tachykinins were reduced after tetrodotoxin (P less than 0.05) and atropine (P less than 0.05) but unchanged after treatment with hexamethonium [40].
• Dextran in lactated Ringer's solution (20 ml/kg) was infused for 1 hour into anesthetized dogs with sinoaortic denervation and vagotomy (deafferentation; n = 10) and dogs treated with hexamethonium (de-efferentation; n = 13) to compare with our previous observation in dogs with an intact autonomic nervous system (control, n = 34) [4].
• Pretreatment with reserpine (1 mg/kg, im, 24 hours before experiments) or hexamethonium (3 mg/kg, iv) prevented the LAD ligation-induced increase in the glycogen phosphorylase activity, but adrenalectomy did not [41].
• Bilateral microinjection of glycine (50 nmol, 100 nL) into the RVLM of hypertensive rats produced a decrease in mean arterial blood pressure (MAP) from 158+/-4 to 71+/-4 mm Hg (P<0.05), which was similar to the decrease produced by intravenous administration of hexamethonium [42].

References