Splenorenal reflex regulation of arterial pressure

During the course of our studies into the control of fluid extravasation from the splenic vasculature, we found that intrasplenic inhibition of NO biosynthesis caused an increase in systemic blood pressure. The present experiments were designed to investigate the mechanisms underlying this novel observation. There was an increase in mean arterial pressure when the nonspecific NO inhibitor N(G)-monomethyl-L-arginine (L-NMMA) was infused via the splenic artery but not when the same dose was administered systemically. Conversely, blood pressure decreased after intrasplenic but not systemic administration of the NO donor S-nitroso-N-acetyl-D,L-penicillamine. There was no pressor response to intrasplenic administration of either the inducible or neuronal NO synthase inhibitors N-[3-(aminomethyl)-benzyl] aceramidine and L-N(5)-(1-imino-3-butenyl)-ornithine. The pressor response to L-NMMA was abolished by denervation of either the spleen or the kidney and by pretreatment with the ACE inhibitor enalapril. We propose that the spleen influences systemic blood pressure through a reflex pathway comprising splenic afferent nerves and renal sympathetic control of renin release.