INTRACEREBROVENTRICULAR INJECTION OF PROSTAGLANDIN E(2) INCREASES SPLENIC SYMPATHETIC-NERVE ACTIVITY IN RATS

The effects of central administration of prostaglandin E(2) (PGE(2)) a nd its selective agonists on splenic sympathetic nerve activity (SNA) were investigated in urethan- and alpha-chloralose-anesthetized rats. An intra-third-cerebroventricular (I3V) injection of PGE(2) (0.1-10 nm ol/kg) increased splenic SNA in a dose-dependent manner. An I3V inject ion of an EP(1) agonist, 17-phenyl-omega-trinor PGE(2) (1-30 nmol/kg), also resulted in a dose-dependent increase in splenic SNA, with a tim e course similar to that of PGE(2)-induced responses. In contrast, EP( 2) agonists, butaprost (10-100 nmol/kg I3V) and 11-deoxy-PGE(1) (10-10 0 nmol/kg I3V), had no effect on splenic SNA. An I3V injection of M & B-28767 (an EP(3)/EP(1) agonist, EP(3) much greater than EP(1)) increa sed splenic SNA only at high doses (10-100 nmol/kg). Pretreatment with an EP(1) antagonist, SC-19220 (200 and 500 nmol/kg), completely block ed the responses of splenic SNA to PGE(2) (0.1 nmol/kg) and M & B-2876 7 (10 nmol/kg), respectively. These findings indicate that brain PGE(2 ) increases splenic SNA through its action on EP(1) receptors.