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Am J Physiol Regul Integr Comp Physiol 269: R662-R668, 1995;
0363-6119/95 $5.00
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AJP - Regulatory, Integrative and Comparative Physiology, Vol 269, Issue 3 662-R668, Copyright © 1995 by American Physiological Society

ARTICLES

Intracerebroventricular injection of prostaglandin E2 increases splenic sympathetic nerve activity in rats

T. Ando, T. Ichijo, T. Katafuchi and T. Hori
Department of Physiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.

The effects of central administration of prostaglandin E2 (PGE2) and its selective agonists on splenic sympathetic nerve activity (SNA) were investigated in urethan- and alpha-chloralose-anesthetized rats. An intra-third-cerebroventricular (13V) injection of PGE2 (0.1-10 nmol/kg) increased splenic SNA in a dose-dependent manner. An I3V injection of an EP1 agonist, 17-phenyl-omega-trinor PGE2 (1-30 nmol/kg), also resulted in a dose-dependent increase in splenic SNA, with a time course similar to that of PGE2-induced responses. In contrast, EP2 agonists, butaprost (10-100 nmol/kg I3V) and 11-deoxy-PGE1 (10-100 nmol/kg I3V), had no effect on splenic SNA. An I3V injection of M & B-28767 (an EP3/EP1 agonist, EP3 >> EP1) increased splenic SNA only at high doses (10-100 nmol/kg). Pretreatment with an EP1 antagonist, SC-19220 (200 and 500 nmol/kg), completely blocked the responses of splenic SNA to PGE2 (0.1 nmol/kg) and M & B-28767 (10 nmol/kg), respectively. These findings indicate that brain PGE2 increases splenic SNA through its action on EP1 receptors.


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