scholarly journals Prostaglandin E2, a Postulated Astrocyte-Derived Neurovascular Coupling Agent, Constricts Rather than Dilates Parenchymal Arterioles

2013 ◽  
Vol 33 (4) ◽  
pp. 479-482 ◽  
Author(s):  
Fabrice Dabertrand ◽  
Rachael M Hannah ◽  
Jessica M Pearson ◽  
David C Hill-Eubanks ◽  
Joseph E Brayden ◽  
...  
Keyword(s):  
Prostaglandin E2 ◽  
Mouse Brain ◽  
Coupling Agent ◽  
Neurovascular Coupling ◽  
Prostaglandin E ◽  
Direct Effects ◽  
Direct Role ◽  
Astrocytic Endfeet

It has been proposed that prostaglandin E2 (PGE2) is released from astrocytic endfeet to dilate parenchymal arterioles through activation of prostanoid (EP4) receptors during neurovascular coupling. However, the direct effects of PGE2 on isolated parenchymal arterioles have not been tested. Here, we examined the effects of PGE2 on the diameter of isolated pressurized parenchymal arterioles from rat and mouse brain. Contrary to the prevailing assumption, we found that PGE2 (0.1, 1, and 5 μmol/L) constricted rather than dilated parenchymal arterioles. Vasoconstriction to PGE2 was prevented by inhibitors of EP1 receptors. These results strongly argue against a direct role of PGE2 on arterioles during neurovascular coupling.

scholarly journals Role of cyclooxygenase-2-mediated prostaglandin E2-prostaglandin E receptor 4 signaling in cardiac reprogramming

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Naoto Muraoka ◽  
Kaori Nara ◽  
Fumiya Tamura ◽  
Hidenori Kojima ◽  
Hiroyuki Yamakawa ◽  
...  
Keyword(s):  
Prostaglandin E2 ◽  
Cyclooxygenase 2 ◽  
Prostaglandin E

scholarly journals Prostaglandin E 2 , a postulated astrocyte‐derived neurovascular coupling agent, constricts rather than dilates parenchymal arterioles

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Fabrice Dabertrand ◽  
Rachael M Hannah ◽  
Jessica M Pearson ◽  
David C Hill‐Eubanks ◽  
Joseph E Brayden ◽  
...  
Keyword(s):  
Coupling Agent ◽  
Neurovascular Coupling ◽  
Prostaglandin E

EFFECT OF PROSTAGLANDIN E2 AND A2 ON STEROID SYNTHESIS BY THE RAT ADRENAL GLAND

1975 ◽  
Vol 65 (1) ◽  
pp. 55-63 ◽  
Author(s):  
A. SPÄT ◽  
SARA JÓZAN
Keyword(s):  
Adrenal Gland ◽  
Prostaglandin E2 ◽  
Adrenal Glands ◽  
Prostaglandin E ◽  
Sodium Restriction ◽  
Aldosterone Secretion ◽  
Steroid Synthesis ◽  
Aldosterone Production ◽  
Hypophysectomized Rats

SUMMARY Prostaglandin E2 increased aldosterone output by superfused capsular adrenal glands obtained from sodium-repleted, hypophysectomized rats but corticosterone did not show a statistically significant increase. Prostaglandin A2 increased corticosterone but not aldosterone production by incubated capsular glands obtained from sodium-repleted, hypophysectomized rats. Both aldosterone and corticosterone production rates were increased by PGA2 after previous sodium restriction. Corticosterone production rate of the decapsulated adrenal gland was not significantly modified by prostaglandin A2 in a concentration effective on the capsular adrenal gland. A possible role of prostaglandins in the regulation of aldosterone secretion is discussed.

scholarly journals The Role of Interleukin-6 in Lipopolysaccharide-Induced Fever by Mechanisms Independent of Prostaglandin E2

Endocrinology ◽  
2008 ◽  
Vol 150 (4) ◽  
pp. 1850-1860 ◽  
Author(s):  
Camilla Nilsberth ◽  
Louise Elander ◽  
Namik Hamzic ◽  
Maria Norell ◽  
Johanna Lönn ◽  
...  
Keyword(s):  
Prostaglandin E2 ◽  
Knockout Mice ◽  
Cyclooxygenase 2 ◽  
Prostaglandin E ◽  
Wild Type ◽  
Febrile Response ◽  
Prostaglandin E Synthase ◽  
Genotype Difference ◽  
The Relationship

Fever has been shown to be elicited by prostaglandin E2 (PGE2) binding to its receptors on thermoregulatory neurons in the anterior hypothalamus. The signals that trigger PGE2 production are thought to include proinflammatory cytokines, such as IL-6. However, although the presence of IL-6 is critical for fever, IL-6 by itself is not or only weakly pyrogenic. Here we examined the relationship between IL-6 and PGE2 in lipopolysaccharide (LPS)-induced fever. Immune-challenged IL-6 knockout mice did not produce fever, in contrast to wild-type mice, but the expression of the inducible PGE2-synthesizing enzymes, cyclooxygenase-2 and microsomal prostaglandin E synthase-1, was similarly up-regulated in the hypothalamus of both genotypes, which also displayed similarly elevated PGE2 levels in the cerebrospinal fluid. Nevertheless, both wild-type and knockout mice displayed a febrile response to graded concentrations of PGE2 injected into the lateral ventricle. There was no major genotype difference in the expression of IL-1β and TNFα or their receptors, and pretreatment of IL-6 knockout mice with soluble TNFα receptor ip or intracerebroventricularly or a cyclooxygenase-2 inhibitor ip did not abolish the LPS unresponsiveness. Hence, although IL-6 knockout mice have both an intact PGE2 synthesis and an intact fever-generating pathway downstream of PGE2, endogenously produced PGE2 is not sufficient to produce fever in the absence of IL-6. The findings suggest that IL-6 controls some factor(s) in the inflammatory cascade, which render(s) IL-6 knockout mice refractory to the pyrogenic action of PGE2, or that it is involved in the mechanisms that govern release of synthesized PGE2 onto its target neurons.

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