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Results for “Piperoxan”

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At least 37 records · Page 2Linked to original sources
PubMed1986

Interaction between central alpha 1- and alpha 2-adrenoceptors on sympathetic tone in rats.

The interaction between piperoxan and alpha 2-agonists on sympathetic tone was studied in rats. The sympatho-inhibitory effect of alpha 2-agonists (clonidine, guanfacine, B-HT 933) was assessed by recording heart rate in normotensive bilaterally-vagotomized rats. Clonidine (3 micrograms/kg, i.c.v.) and B-HT 933 (100 micrograms/kg, i.c.v.) induced a bradycardia which was fully reversed by piperoxan (30 micrograms/kg, i.c.v.). However, in rats treated with guanfacine, piperoxan induced a partial recovery of the bradycardic effect. The injection of a small dose of the specific alpha 1-adrenoceptor blocking drug, AR-C 239 (10 micrograms/kg, i.c.v.) which, by itself did not modify heart rate, completely inhibited the reversal effect of piperoxan in rats treated with clonidine, B-HT 933 or guanfacine. In rat brainstem membranes, B-HT 933 was found to bind to both alpha 1- and alpha 2-adrenoceptors and was as potent as clonidine in competing for alpha 1-sites bound by [3H]prazosin. On the other hand, in bilaterally vagotomized rats, piperoxan (30 micrograms/kg, i.c.v.) induced an increase in blood pressure and heart rate which was inhibited by previous administration of AR-C 239 (10 micrograms/kg, i.c.v.). These data suggest that, by inhibiting central alpha 2-adrenoceptors, piperoxan unmasks central alpha 1-adrenoceptor stimulation by endogenous catecholamines leading to an increase in the sympathetic tone, but a full recovery in heart rate could be observed only with the mixed alpha 1- and alpha 2-adrenoceptor agonists, clonidine and B-HT 933. In addition, these data further indicate that alpha 1-adrenoceptors are implicated in a tonic control of the sympathetic nerve activity in normotensive rats.

Animals↗
PubMed1983

Evidence for a central sympathoexcitatory action of alpha-2 adrenergic antagonists.

The effect of alpha-2 adrenergic receptor antagonists on sympathetic nerve discharge (SND) recorded from the external carotid and splanchnic nerves were studied in baroreceptor-denervated cats. Low i.v. doses of piperoxane and rauwolscine dramatically increased SND and produced a concomitant rise in mean arterial pressure and heart rate. High doses of piperoxane also resulted in an increase in SND. High doses of rauwolscine, however, markedly reduced mean arterial pressure, heart rate and SND. The pressor response to i.v. norepinephrine was greatly attenuated by high doses of rauwolscine and slightly reduced by piperoxane. Piperoxane failed to alter SND in catecholamine-depleted animals. In vitro binding experiments indicated that piperoxane and rauwolscine bound selectively to the alpha-2 adrenergic receptor and had little affinity for alpha-1 receptor sites. In addition, rauwolscine displaced [3H]LSD binding. These data indicate that low doses of the alpha-2 receptor antagonist piperoxane and rauwolscine act centrally to increase SND. In addition, the nature of the interactions between central noradrenergic neurons and neurons involved in the genesis of sympathetic nerve activity is discussed.

Adrenergic alpha-Antagonists↗
PubMed1981

Increased ouabain binding after repeated noradrenergic stimulation.

Acute noradrenergic stimulation has previously been shown to stimulate brain (Na+, K+)-adenosine triphosphatase activity. Effects of repeated stimulation with piperoxane were examined in the present study. Daily piperoxane increased ouabain binding, measured 24 h after the last dose, after 4 days or 3 weeks treatment; K+-p-nitrophenylphosphatase was increased after 3 weeks. Prazosin, which, like piperoxane, activates presynaptic noradrenergic neurons but, unlike piperoxane, blocks postsynaptic receptors, did not increase K+-p-nitrophenylphosphatase, and decreased ouabain binding after 3 weeks.

4-Nitrophenylphosphatase↗