Disease relevance of Benodaine

• Piperoxane (10 and 20 mg/kg, IP) significantly potentiated PTZ-induced tonic seizures and mortality [1].
• Piperoxan (150 micrograms/kg i.v. or 10 micrograms/kg i.a. vert.) given 15 min after St 91 (16 micrograms/kg i.a. vert.) reduced both the hypotension and bradycardia [2].
• Infusion of St 91 (4--16 microgram/kg over 2 min) into the vertebral artery (i.a. vert.) produced dose-dependent hypotension and bradycardia only, which were reversed by piperoxan (300 microgram/kg, intracisternal) [3].
• Hypothermia was inhibited by piperoxan injected intracisternally (10 millimicron/kg) but not intraperitoneally (10 and 50 millimicron/kg) [4].
• S 3341 reduced the tachycardia resulting from stimulation of the cardioaccelerator nerve in the anaesthetized, spinalised and bilateraly vagotomised dog, this effect was reversed by piperoxan [5].

Psychiatry related information on Benodaine

• Phenoxybenzamine and prazosine did not antagonize the anti-withdrawal effect of clonidine, whereas piperoxane and yohimbine were effective with respect to locomotor activity and a total abstinence score [6].
• A larger dose of piperoxane (45 mg/kg) and graded doses of phentolamine and PBZ, affecting both pre- and post-synaptic receptors, depressed self-stimulation, and did not antagonize clonidine-induced depression of self-stimulation [7].

High impact information on Benodaine

• The direct effect of alpha 2-autoreceptors was studied by measuring the effects of piperoxan, an alpha 2-autoreceptor antagonist, and clonidine, an agonist on catecholamine exocytosis, from single bovine chromaffin cells in culture [8].
• Administration of the alpha 2-adrenoceptor antagonist piperoxane failed to produce any changes in either of these parameters, suggesting that at least in vitro the afterhyperpolarization and postactivation inhibition seen in locus coeruleus neurons do not result from the activation of alpha 2-adrenoceptors [9].
• The comparison of long-term change in tyrosine hydroxylase values after piperoxane, RU24722, clonidine, and combined RU24722-clonidine treatment demonstrated that an activation during a few hours did not induce tyrosine hydroxylase in central noradrenergic neurons [10].
• This PRL increase was maximal 15 min after piperoxane infusion and significant, when compared with baseline levels, in the +15, +30, +45, +60, and +90-min samples [11].
• Thus, infusion into the locus coeruleus of the alpha-2 agonist clonidine, but not the alpha-2 antagonist piperoxane, eliminated behavioral depression.(ABSTRACT TRUNCATED AT 250 WORDS)[12]

Chemical compound and disease context of Benodaine

• The baroreflex bradycardia induced by volume loading as abolished by yohimbine and piperoxan but not by phenoxybenzamine, microinjected bilaterally into the nucleus ambiguus [13].
• 4. p-Octopamine hypotension was not antagonized by piperoxan, yohimbine and prazosin, a relatively selective antagonist of post-synaptic alpha adrenoceptors [14].
• 4 The clonidine-induced bradycardia was antagonised by prazosin, WB4101, piperoxan or yohimbine [15].

Biological context of Benodaine

• Low i.v. doses of piperoxane and rauwolscine dramatically increased SND and produced a concomitant rise in mean arterial pressure and heart rate [16].
• Brainstem mechanisms in the modulation of the sympathetic baroreflex by piperoxan [17].
• Piperoxan (5 micrograms) injected bilaterally into the ventrolateral pressor area did not change blood pressure or the rate of sympathetic discharge [17].
• The alpha 2-adrenoceptor antagonists piperoxan and idazoxan inhibited the yawning response without affecting the penile erections [18].
• Apart from piperoxan and its analogues, which showed some preference for alpha 2-adrenergic binding sites, all benzodioxane-like structures displayed a general selectivity for the alpha 1-adrenoreceptor sites labeled with 3H-prazosin [19].

Anatomical context of Benodaine

• 5-MeOT-induced hindlimb scratching could be inhibited dose dependently by the alpha 2-adrenoceptor blockers yohimbine and rauwolsince, which also have high affinity for 5-HT1D receptors, whereas the alpha 2-adrenoceptor blocker piperoxan only weakly counteracted hindlimb scratching [20].
• Piperoxan (50-100 micrograms/kg) injected into the cisterna magna of anaesthetized dogs increased blood pressure, heart rate and resting rate of sympathetic nerve discharge [17].
• Piperoxan (5 micrograms) injected bilaterally into the nucleus tractus solitarii (NTS) increased blood pressure and resting sympathetic nerve activity with a shift of the sympathetic baroreflex curve to the right and no change in baroreflex sensitivity [17].
• 3. The accumulation of Dopa after decarboxylase inhibition cranial to a lesion of the spinal cord was accelerated by yohimbine, piperoxan and tolazoline, but not significantly affected by phenoxybenzamine and haloperidol (10 mg/kg) [21].
• Taking the levels of the DA metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) as a measure of the rate of DA turnover, it was found that prazosin and phenoxybenzamine decreased, whereas piperoxane and yohimbine increased the turnover rate both in the corpus striatum and in the tuberculum olfactorium [22].

Associations of Benodaine with other chemical compounds

• When infused into the locus coeruleus region, small doses of the antagonists piperoxane and yohimbine depressed activity in the swim test while infusion of the agonists clonidine and NE had the opposite effect of stimulating activity [23].
• Antagonism of pressor responses to sympathetic outflow stimulation and alpha-adrenoceptor agonists in pithed spontaneously hypertensive rats was used to estimate postsynaptic alpha-adrenoceptor blocking activity of mianserin, phentolamine, phenoxybenzamine, piperoxan and yohimbine [24].
• Noradrenergic neurons of the locus coeruleus: inhibition by epinephrine and activation by the alpha-antagonist piperoxane [25].
• Chronic administration of clorgyline, like acute doses of this MAO A inhibitor, significantly decreases cell firing in the LC and the effect is partially reversed by piperoxane [26].
• The pressor response to stimulation of this hypothalamic area was inhibited when the hypothalamus was superfused with drugs blocking either alpha-adrenoreceptors (piperoxan, tolazoline), or beta-adrenoreceptors--(+/-)-propranolol, (-)-propranolol, practolol, sotalol, metoprolol [27].

Gene context of Benodaine

• It has been suggested that the stimulation of the secretion of PRL by the alpha 2 adrenergic receptor antagonists (yohimbine, piperoxane) results from blockade of an inhibitory influence imposed on PRL release by the central alpha 2 receptors (7, 15) [28].
• However, the alpha 2 antagonists yohimbine and piperoxan, the alpha 2 agonists medetomidine, guanfacine, and guanabenz, the non-specific alpha antagonist phentolamine, and the alpha 1 antagonist prazosin did not disinhibit conflict responding in the Vogel lick-shock paradigm [29].
• S 3341 reduced hypertension and tachycardia due to stimulation of the sympathetic outflow in the pithed rat, an effect also antagonised by piperoxan [5].

Analytical, diagnostic and therapeutic context of Benodaine

• Similarly, microinjection of the alpha-2 adrenergic antagonist piperoxan (10 nmol) decreased the duration (from 45 +/- 8 to 23 +/- 4 min), but not the magnitude of the sympathoinhibitory response [30].
• 2 At concentrations greater than 2 x 10(-4) M, piperoxan produced a rise in perfusion pressure, a contraction of the splenic capsule, and a marked dose-dependent decrease in transmitter overflow [31].
• A capillary electrophoresis (CE) study of the separation of Piperoxan enantiomers was carried out in order to find the buffer conditions that produce the maximum peak separation time between the two enantiomers and the optimal chiral selector concentration [32].
• Prazosin, a specific post-synaptic alpha 1 adrenoceptor blocker, induced hypothermia whereas piperoxan (presynaptic alpha 2 antagonist) produced hyperthermia [33].
• The inhibitory effects produced by iontophoresis of alpha-MNE or Clo were reduced to the same degree (86-98%) by iontophoresis of idazoxan (an alpha 2-adrenergic antagonist with imidazoline structure) and by iontophoresis of piperoxan (65-77%, a nonimidazoline alpha 2-antagonist) [34].

References