Roles of nitric oxide in the spinal cord in cardiovascular regulation in rats

The roles of nitric oxide (NO) in the spinal cord in regulation of blood pressure were examined in anesthetized rats. Intrathecal (i.t.) injection of an inhibitor of NO synthase (NOS), N(omega)-nitro-L-arginine methylester (L-NAME), caused marked dose-dependent increase in the blood pressure. The pressor response to L-NAME was attenuated by pretreatment with L-arginine (10 micromol, i.t.). Pretreatment with the ganglionic blocker pentolinium (10 mg/kg, i.v.) and alpha1- and beta-adrenoceptor antagonists significantly inhibited the pressor response induced by L-NAME. The pressor responses to L-NAME was blocked by pretreatment with the selective N-methyl-D-aspartate (NMDA) receptor antagonist DL-2-amino-5-phosphonovaleric acid (AP-5) (50 nmol, i.t.), but not by pretreatment with a non-NMDA receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). In addition, the pressor response to L-NAME was reduced by spinal cord transection. These results suggest that L-NAME causes activation of the sympathetic nervous system by reduction of NO in the spinal cord, and that this reduction of NO by L-NAME may activate glutamatergic neurons in the medulla oblongata.