Effects of centrally administered prostaglandin E3 and thromboxane A3 on plasma noradrenaline and adrenaline in rats: Comparison with prostaglandin E2 and thromboxane A2

Abstract

Previously, we reported the involvement of brain -6 prostanoids, especially prostaglandin E 2 and thromboxane A 2 , in the activation of central sympathoadrenomedullary outflow in rats. -3 Prostanoids, including prostaglandin E 3 and thromboxane A 3 , are believed to be less bioactive than -6 prostanoids, although studies on the functions of -3 prostanoids in the central nervous system have not been reported. In the present study, therefore, we compared the effects of centrally administered -3 prostanoids, prostaglandin E 3 and thromboxane A 3 , with those of -6 prostanoids, prostaglandin E 2 and thromboxane A 2 , on the plasma catecholamines in anesthetized rats. Intracerebroventricularly (i.c.v.) administered prostaglandin E 2 (0.15, 0.3 and 1.5 nmol/animal) and prostaglandin E 3 (0.3 and 3 nmol/animal) predominantly elevated plasma noradrenaline but not adrenaline, but the latter was less efficient than the former. On the other hand, U-46619 (an analog of thromboxane A 2 ) (30, 100 and 300 nmol/animal, i.c.v.) and ∆ 17 -U-46619 (an analog of thromboxane A 3 ) (100 and 300 nmol/animal, i.c.v.) both elevated plasma catecholamines (adrenaline >> noradrenaline) to the same degree. These results suggest that centrally administered prostaglandin E 3 is less effective than prostaglandin E 2 to elevate plasma noradrenaline, and that thromboxane A 3 is almost as equipotent as thromboxane A 2 to elevate plasma catecholamines in rats.3

Stimulatory and Inhibitory Roles of Brain 2-Arachidonoylglycerol in Bombesin-Induced Central Activation of Adrenomedullary Outflow in Rats

“…Takahiro Shimizu 1, *, Kenjiro Tanaka 1 , and Kunihiko Yokotani nisms, elevated plasma levels of catecholamines in rats (7,8). These results suggest that the cyclooxygenasemediated production of active arachidonic acid metabolites (prostanoids) in the brain is involved in the bombesin-induced activation of central adrenomedullary outflow in rats.…”

Palmitoleic Acid Inhibits RANKL-Induced Osteoclastogenesis and Bone Resorption by Suppressing NF-κB and MAPK Signalling Pathways

“…FAs are commonly found in nuts, oils, seafood, and various other widely consumed food sources. Several studies have focused on the importance of unsaturated FAs in bone metabolism [8,10,11,28,29,30,31]. Chronic inflammatory diseases are known to increase the risk of bone fractures, as pro-inflammatory cytokines amplify the formation of osteoclasts [32].…”