Role of brain thromboxane A2 in the release of noradrenaline and adrenaline from adrenal medulla in rats

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

“…Previously, we reported that bilateral adrenalectomy abolished the elevation of plasma noradrenaline and adrenaline induced by centrally administered vasopressin, bombesin and histamine (Okada et al, 2003;Yokotani et al, 2005;Shimizu et al, 2006). In the present study, bilateral adrenalectomy abolished the centrally administered epibatidine-induced elevation of both plasma noradrenaline and adrenaline.…”

“…Previously, we reported that central pretreatment with indomethacin or ketoprofen (inhibitors of cyclooxygenase) attenuated the centrally administered CRF-, vasopressin-, histamine-, GLP-1-and bombesin-induced elevation of plasma noradrenaline and adrenaline (Okada et al, 2003;Shimizu et al, 2006;Arai et al, 2008;Lu et al, 2008), suggesting the involvement of the brain prostanoids in these substances-induced elevation of plasma catecholamines in rats. In the present study, central pretreatment with indomethacin effectively attenuated the elevation of plasma noradrenaline and adrenaline induced by centrally administered epibatidine.…”

“…We previously reported that centrally administered prostaglandin E 2 (but not prostaglandin D 2 , I 2 and F 2alpha ) elevates plasma noradrenaline from sympathetic nerves by activation of the brain prostanoid EP 3 receptors in rats (Yokotani et al, 1995(Yokotani et al, , 2005Murakami et al 2002) and also that microinjection of thromboxane A 2 mimetic into the hypothalamic paraventricular nucleus predominantly elevates plasma adrenaline by activation of the brain prostanoid TP receptors in rats (Murakami et al, 2002). Furthermore, the brain prostanoid TP receptors are involved in the centrally administered vasopressin-, bombesin-and histamine-induced secretion of both noradrenaline and adrenaline from noradrenalineand adrenaline-containing cells in the adrenal medulla and in the centrally administered CRF-and GLP-1-induced secretion of adrenaline from adrenalinecontaining cells in the adrenal medulla in rats (Okada et al, 2003;Yokotani et al, 2005;Shimizu et al, 2006;Arai et al, 2008). The activation of brain TP receptors has been shown to elevate blood pressure and plasma catecholamines in hemorrhaged hypotensive rats (Yalcin and Savci, 2004).…”

“…We recently reported that centrally administered stress-related neurotransmitters such as vasopressin, bombesin and histamine elicit adrenal secretion of both noradrenaline and adrenaline from noradrenaline-and adrenaline-containing cells in the adrenal medulla via the brain thromboxane A 2 -mediated mechanisms, whereas centrally administered corticotropin-releasing factor (CRF) and glucagon-like peptide 1 (GLP-1) elicits adrenaline secretion from adrenal adrenaline-containing cells and noradrenaline release from sympathetic nerves via the brain thromboxane A 2 -and prostaglandin E 2 -mediated mechanisms, respectively, in rats (Okada et al, 2003;Yokotani et al, 2005;Shimizu et al, 2006;Arai et al, 2008). In the present study, therefore, we examined the mechanisms involved in the centrally administered epibatidine (a potent agonist of nicotinic acethylcholine receptors)-induced elevation of plasma catecholamines with regard to the brain prostanoids using urethaneanesthetized rats.…”

Possible inhibitory roles of endogenous 2-arachidonoylglycerol during corticotropin-releasing factor-induced activation of central sympatho-adrenomedullary outflow in anesthetized rats

“…Recently, we reported the involvement of brain arachidonic acid generated by brain phospholipase C-, diacylglycerol lipase-and monoacylglycerol lipase-mediated mechanisms in centrally administered arginine-vasopressin-induced elevation of plasma noradrenaline and adrenaline in rats (Shimizu et al, 2004;Shimizu and Yokotani, 2008). Brain arachidonic acid has already been shown to be involved as a precursor of prostanoids in this peptide-induced elevation of plasma catecholamines (Yokotani et al, 1995(Yokotani et al, , 2000Murakami et al, 2002;Okada et al, 2003a). Furthermore, it is interesting to note that 2-arachidonoylglycerol, a precursor of arachidonic acid, plays a modulating role as an endocannabinoid to inhibit the arginine-vasopressin-induced response (Shimizu and Yokotani, 2008).…”