Brain cyclooxygenase and prostanoid TP receptors are involved in centrally administered epibatidine-induced secretion of noradrenaline and adrenaline from the adrenal medulla in rats

Abstract

Plasma adrenaline mainly originates from adrenaline-containing cells in the adrenal medulla, whereas plasma noradrenaline reflects not only the release from sympathetic nerves but also the secretion from noradrenaline-containing cells in the adrenal medulla. The present study was undertaken to examine the mechanisms

Possible inhibitory role of endogenous 2-arachidonoylglycerol as an endocannabinoid in (±)-epibatidine-induced activation of central adrenomedullary outflow in the rat

“…dose-dependently elevated plasma levels of catecholamines (noradrenaline and adrenaline) in the rat (Shimizu and Yokotani, 2009), therefore, we used the smallest dose of 1 nmol to examine the potentiating effect of a CB 1 receptor antagonist on the elevation of plasma levels of catecholamines. Treatments with vehicle-1 (3 ml DMF/animal, i.c.v.)…”

“…Centrally administered (À)-nicotine also induces a pressor response and an elevation of plasma catecholamines by activation of brain nicotinic acetylcholine receptors (Buccafusco and Yang, 1993;Kiritsy-Roy et al, 1990;Tseng et al, 1993). We reported that centrally administered (±)-epibatidine, a non-selective agonist of nicotinic acetylcholine receptors (Lembeck, 1999), evoked both catecholamines secretion from the adrenal medulla by activation of brain a4b2 nicotinic acetylcholine receptors in the rat (Shimizu and Yokotani, 2009;Shimizu et al, 2011b). Furthermore, the (±)-epibatidineinduced response was reduced by centrally pretreated indomethacin (Shimizu and Yokotani, 2009), a cyclooxygenase inhibitor, and the pretreatment also suppressed plasma catecholamines elevation induced by centrally administered arachidonic acid (AA), a representative substrate for cyclooxygenase in the rat (Yokotani et al, 2000a).…”

“…We reported that centrally administered (±)-epibatidine, a non-selective agonist of nicotinic acetylcholine receptors (Lembeck, 1999), evoked both catecholamines secretion from the adrenal medulla by activation of brain a4b2 nicotinic acetylcholine receptors in the rat (Shimizu and Yokotani, 2009;Shimizu et al, 2011b). Furthermore, the (±)-epibatidineinduced response was reduced by centrally pretreated indomethacin (Shimizu and Yokotani, 2009), a cyclooxygenase inhibitor, and the pretreatment also suppressed plasma catecholamines elevation induced by centrally administered arachidonic acid (AA), a representative substrate for cyclooxygenase in the rat (Yokotani et al, 2000a). These results suggest that brain cyclooxygenasemediated production of AA metabolites is involved in the (±)-epibatidine-induced activation of central adrenomedullary outflow.…”

Stimulation of brain nicotinic acetylcholine receptors activates adrenomedullary outflow via brain inducible NO synthase‐mediated S‐nitrosylation

“…All other reagents were of the highest grade available (Sigma Aldrich Fine Chemicals). The dosage of drugs was determined according to previous studies (Murakami et al, 1998;Lu et al, 2008;Pei et al, 2008;Shimizu and Yokotani, 2009;Tanaka et al, 2012) and our preliminary experiments.…”

“…All values are expressed as means ± SEM. The sample size in each experimental group for blood sampling was determined based on the expected difference in a desired endpoint measurement among the test and control groups, and the mean of the SDs for the groups observed in our previous studies (Shimizu and Yokotani, 2009;Shimizu et al, 2011). In the experiments consisting of 16 groups of rats, six rats per group were used at first for collection of blood samples.…”