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At least 19 recordsLinked to original sources
PubMed1978

The effects of piperoxan on uptake of noradrenaline and overflow of transmitter in the isolated blood perfused spleen of the cat.

1 The competitive alpha-adrenoceptor blocking agent, piperoxan, in concentrations up to 2 x 10(-4) M, produced large dose-dependent increases in transmitter overflow from the isolated blood perfused spleen of the cat following nerve stimulation at 10 hertz. 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. 3 Phenoxybenzamine (10(-4) M) and desmethylimipramine (3 x 10(-5) M) produced further increases in transmitter overflow when added after piperoxan. 4 Piperoxan (5.8 to 6.6 x 10(-6) M) had no effect on the recovery of 3H in the venous blood following the close arterial infusion or injection of (3H)-(--)-noradrenaline, indicating that the drug does not inhibit uptake of the amine. 5 Piperoxan produced dose-dependent inhibition of responses of the splenic vasculature to close arterial injection of 1 microgram of (--)-noradrenaline but was much less effective at inhibiting responses to nerve stimulation. At 2 x 10(-6) M piperoxan produced a considerable reduction of the response to injected noradrenaline but potentiated the response to nerve stimulation. 6 In isolated strips of cat splenic capsule, piperoxan produced a shift to the right of the dose-response curve to noradrenaline with no change of the maximum response. There was no evidence of a postsynaptic sensitizing effect of the type observed in the rat vas deferens.

Animals↗
PubMedDate not supplied

[Comparative study of piperoxan and 2-(2-imidazolinyl)-1, 4-benzodioxane (170 150) on pre- and postsynaptic receptors in the rat].

1. 170 150 (imidazolinyl-2)-2-benzodioxane 1-4), as does piperoxan, competitively antagonizes the hypertension induced by clonidine in the pithed rat. Piperoxan appears slightly less potent than 170 150 in this preparation as shown by the comparison of the apparent pA10 values: 5.3 for piperoxan versus 5.4 for 170 150. 2. The two drugs antagonize the reduction of the electrically-induced tachycardia produced by clonidine. 170 150 appears to be 3-fold more potent than piperoxan in this preparation. 3. These results are compatible with a blockade of alpha 2-pre and postsynaptic adrenoceptors of the rat by piperoxan and 170 150 appears to be 3-fold more potent than piperoxan in this preparation. 3. These results are compatible with a blockade of alpha 2-pre and postsynaptic adrenoceptors of the rat by piperoxan and 170 150 and they are in agreement with our previous results which indicate that compound 170 150 shows a preferential affinity for alpha 2-adrenoceptors.

Animals↗
PubMed1988

Brainstem mechanisms in the modulation of the sympathetic baroreflex by piperoxan.

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. The baroreflex curve was shifted to the right with an elevation of the upper plateau (when blood pressure was lowered below resting values, renal sympathetic nerve activity rose to an upper plateau) and with no change in baroreflex sensitivity. Catecholamine depletion, produced by reserpine and alpha-methyl-p-tyrosine, did not change the effects of piperoxan on resting sympathetic nerve activity and on the baroreflex curve. Piperoxan (50 micrograms/kg i.c.) enhanced the rate of renal sympathetic nerve discharge in baroreceptor-denervated dogs. 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. Piperoxan (5 micrograms) injected bilaterally into the ventrolateral pressor area did not change blood pressure or the rate of sympathetic discharge. However, the baroreflex curve was shifted to the right with an elevation of the upper plateau level and the baroreflex sensitivity was increased. The present findings suggest that tonically active alpha 2-adrenergic mechanisms located within the NTS regulate resting and reflex sympathetic activity. An alpha 2-adrenergic mechanism in the rostral ventrolateral medulla modulates reflex sympathetic activity but has no influence on resting activity.

Animals↗
PubMed1984

Effects of clonidine, piperoxane and locus coeruleus lesion on the serotonergic and dopaminergic systems in raphe and caudate nucleus.

To assess the influences of central noradrenergic neurons on both serotonergic and dopaminergic systems, the neurochemical effects of clonidine, piperoxane, and 6-hydroxydopamine were examined. Using quantitative fluorescence histochemistry and high performance liquid chromatography, we have demonstrated that clonidine, much like apomorphine, preferentially augmented intracellular serotonin (5-HT) fluorescence in the dorsal raphe without affecting 5-HT cells in the median raphe nucleus. Clonidine also produced a significant decrease of extraperikaryal catecholamine (CA) fluorescence in the same region. Piperoxane, at a dose having no significant effect alone, antagonized the effects of clonidine on 5-HT and CA. 6-Hydroxydopamine lesions of the locus coeruleus produced a similar increase of 5-HT fluorescence in the dorsal raphe and decrease of CA fluorescence in both the dorsal and median raphe. Biochemically, clonidine decreased while piperoxane increased a measure of 5-HT turnover in the corresponding terminal region of the dorsal raphe, the striatum. Similarly, dopamine turnover was also decreased by clonidine and increased by piperoxane in the striatum. These effects may be mediated by noradrenergic projections from the locus coeruleus to both the dorsal raphe and the substantia nigra. These results support the hypothesis that the effects of clonidine on serotonergic and dopaminergic neurons are indirectly mediated through noradrenergic receptor stimulation.

Animals↗
PubMed1978

Effect of piperoxane on serum prolactin: possible role of epinephrine-mediated synapses in the inhibition of prolactin secretion.

Intravenous administration of 2,5 mg/kg piperoxane produced a rapid and significant increase in serum PRL concentrations in four non-human primates. 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. The iv administration of 5 mg/kg piperoxane also produced a rapid and significant increase, whereas saline 0.5 mg/kg or 1.0 mg/kg, did not change serum PRL levels. The iv administration of 10 microgram/kg clonidine, but not saline, produced a rapid and significant reduction in serum PRL levels. PRL levels were significantly reduced +15, +30, and +60 min after the clonidine infusion. Pretreatment with a bolus of 10 microgram/kg clonidine at -15 min caused a significant attenuation of the piperoxane-induced elevation in serum PRL in two monkeys. These data support the hypothesis that alpha-adrenergic receptors are involved in the inhibition of PRL secretion. These data are compatible with noradrenergic or adrenergic mechanisms which remain to be defined.

Animals↗
PubMed1977

Presynaptic alpha-adenoceptors: the depression of self-stimulation by clonidine and its restoration by piperoxane but not by phentolamine or phenoxybenzamine.

Depression of self-stimulation by clonidine has been ascribed to continuous direct stimulation of alpha-adrenoceptors with consequent disruption of reinforcement signals thought to be conveyed by noradrenergic pathways. This suggestion was tested by administration of alpha-receptor blocking agents (piperoxane, phentolamine and phenoxybenzamine, PBZ) differing in their affinity for pre- and post-synaptic receptor sites. Piperoxane in low doses (0.55-5.0 mg/kg) previously reported to cause specific blockade of pre-synaptic receptors implicated in negative feedback circuits, caused a significant increase in self-stimulation rate and strongly antagonized the depression of self-stimulation by clonidine (0.15 mg/kg). 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. It is concluded that depression of self-stimulation by clonidine may depend on clonidine-induced inhibition of NA release exerted via presynaptic receptors, and that the effect of clonidine is not necessarily evidence that noncontingent adrenergic stimulation disrupts reinforcement.

Animals↗
PubMed1978

Piperoxane reduces the effects of clonidine on aggression in mice and on noradrenaline dependent hypermotility in rats.

Aggression in isolated male mice and hypermotility in rats produced by the noradrenaline releaser H 77/77 were studied after the s.c. administration of the alpha-adrenergic agonist clonidine and the alpha-antagonist piperoxane. Clonidine 0.005--0.5 mg/kg inhibited both behaviours while piperoxane showed a weak and short-lasting antiaggressive effect and no H 77/77 antagonism. Inactive doses of piperoxane reduced the inhibitory effects of clonidine. The results indicate that isolation-induced aggression in mice and H 77/77-induced hypermotility in rats are behavioural signs related to the availability of noradrenaline at the receptor.

Aggression↗
PubMed1982

Effects of prazosin and piperoxan on central cardiovascular actions of St 91 in cats.

Intravenous administration of St 91 (2-(2,6-diethylphenylimino)-imidazolidine hydrochloride) (8 and 16 micrograms/kg) to anaesthetized cats, produced a dose-related but brief rise in blood pressure accompanied by bradycardia. The bradycardia was biphasic. An initial rapid fall in heart rate accompanied the pressor response and was followed by a less pronounced residual bradycardia that long outlasted the pressor response. Prazosin (5 micrograms/kg i.v.) reduced both the mean resting blood pressure and the maximum pressor response to St 91 (8 and 16 micrograms/kg i.v.) and unmasked a small secondary hypotension. The bradycardia was not diminished. Atropine (1 mg/kg i.v.) did not alter the pressor response to St 91 (16 micrograms/kg i.v.) but depressed the initial bradycardia accompanying the pressure rise. The residual bradycardia was not reduced. Piperoxan (150 micrograms/kg i.v. or 10 micrograms/kg i.a. vert.), given after St 91 (16 micrograms/kg i.v.) abolished the residual bradycardia whereas pretreatment with piperoxan (150 micrograms/kg, intracisternally) inhibited both the initial and the residual bradycardia. St 91 (8 and 16 micrograms/kg i.a. vert.) caused hypotension and bradycardia. Prazosin (5 micrograms/kg i.a. vert.) inhibited the hypotension only, but the same dose i.v. was ineffective. 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. The results show that the long-lasting residual bradycardia caused by i.v. St 91 is due to activation of central alpha-adrenoceptors. Selective inhibition of the St 91 (i.a. vert.) hypotension by prazosin may indicate that different receptors mediate hypotension and bradycardia but more likely shows that the central pathways differ.

Animals↗
PubMed1995

Influence of the alpha 2 noradrenergic antagonist piperoxane on longevity in the Fischer-344 rat: a preliminary report.

Piperoxane is an alpha 2-noradrenergic antagonist with demonstrated excitatory effects on neurons in the locus coeruleus, causing a corresponding increase in norepinephrine in many forebrain areas. 16 male Fischer-344 rats approximately 16 months of age were injected with 3 mg/kg of piperoxane or .09% saline. The piperoxane-treated rats lived an average of 127.1 days longer than the saline-treated rats. The results are discussed in terms of the effects of strategies designed to enhance brain levels of catecholamine and their effect on the aging process. A discussion of further research is also presented.

Adrenergic alpha-Antagonists↗
PubMed1994

The alpha-2 antagonists idazoxan and rauwolscine but not yohimbine or piperoxan are anxiolytic in the Vogel lick-shock conflict paradigm following intravenous administration.

The alpha 2 agonist clonidine has been shown to be anxiolytic in a number of preclinical anxiety models. Interestingly, intravenous infusion of the alpha 2 antagonists idazoxan at 10 mg/kg and rauwolscine at 2.24 mg/kg significantly disinhibited lick-shock conflict responding in rats similar to the alpha 2 agonist clonidine (0.022 mg/kg) and the benzodiazepine diazepam (0.5 mg/kg). 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. In fact, yohimbine has been shown to be anxiogenic in both animals and man. This may be due to yohimbine's lack of specificity and its ability to inhibit GABAergic release. In addition, all of these agents, except idazoxan, did not increase water consumption in water deprived rats. Idazoxan (10 mg/kg) significantly decreased water consumption by 45%. Therefore, idazoxan increased conflict responding for water reward at a dose (10 mg/kg) which also decreased water consumption in a non-conflict paradigm. These data suggest that agents with selective antagonism at the alpha 2 receptor site may be anxiolytic while agents with less specificity at this site such as yohimbine, piperoxan, and phentolamine are not anxiolytic.

Adrenergic alpha-Agonists↗
PubMed2000

Continuous free flow electrophoresis for preparative chiral separations of piperoxan using sulfated beta-cyclodextrin.

Continuous free flow electrophoresis was investigated as a tool for the preparative chiral separation of piperoxan using a sulfated cyclodextrin chiral additive. In the absence of chiral additive, the sample stream was deflected cathodically. However, the presence of sulfated cyclodextrin in the run buffer caused anodic deflection and splitting of the sample stream into two streams, each enriched in one enantiomer. Although the sulfated cyclodextrin used was comprised of a mixture of homologues and isomers, this polydispersity did not seem to significantly impact band dispersion. Sample introduction rates ranged from approximately 0.9-7.2 mg h-1. Maximum resolution was 0.53, using an applied voltage of 220 V, buffer composition of 0.075% sulfated cyclodextrin, 7.6 mM citrate (pH 3), 4.5 degrees C.

Adrenergic alpha-Antagonists↗
PubMed1994

Relationship between tyrosine hydroxylase content and noradrenergic cell reactivity to piperoxane: an in vivo voltammetric approach in the rat locus coeruleus.

A previous electrochemical study showed that the increase in the tyrosine hydroxylase (TH) content of the locus coeruleus (LC) produced by RU24722 administration was associated with a relative decrease in the catecholaminergic metabolic reactivity of this nucleus to a hypotensive stimulus. Since alpha 2 receptors participate in the regulation of the activity of both LC neurons and TH, the aim of the present work was to evaluate the possible involvement of the autoinhibition mediated by alpha 2 autoreceptors in the inverse relationship between the reactivity of the LC and its TH content. Our study was divided into two successive steps: (i) the electrochemical measurement of the in vivo metabolic activation of LC cells in response to alpha 2-adrenergic receptor blockade, and (ii) the evaluation of the quantity of TH every 100 microns along the caudorostral axis in each recorded LC. The capacity of TH protein to be activated was evaluated by the measurement, using differential normal pulse voltammetry, of the in vivo variations of the extracellular 3,4-dihydroxyphenylacetic acid concentrations in response to six cumulated doses of the alpha 2-antagonist piperoxane. The corresponding dose-response curves, determined in control- and RU24722-treated rats, were expressed as a function of the quantity of TH contained either in the whole recorded LC or in the 100 microns-wide coronal interval surrounding the recording site. It was established that the slopes of the dose-response curves were significantly (P < 0.01) and inversely related to the quantity of TH at the level of the recording site. This result suggests that the negative control of the catecholaminergic metabolic reactivity in a restricted area of the LC could be directly or indirectly dependent on the level of expression of TH protein in this particular area.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1986

Synthesis and pharmacological evaluation of cyclic and opened thioanalogues of piperoxan.

Three piperoxan analogues, derived from the opening of the benzodioxane ring and/or replacement of the oxygen atom with the less polar sulfur, were synthesized. The decrease of the alpha-blocking activity found for these compounds showed that the binding site of benzodioxane-like compounds does not accept the substitution with less polar groups.

Adrenergic alpha-Antagonists↗