Possible participation of spinal nitric oxide in the control of the blood pressure in anesthetized rats

In pentobarbital-anesthetized rats the intrathecal (i.t.) injection of the nitric oxide (NO) precursor, L-arginine (10 and 20 mu mol), elicited a decrease in the mean blood pressure (MBP) whereas the inhibitor of the NO synthase (NOS) NG-nitro-L-arginine methyl ester (L-NAME; 0.1-10 mu mol) produced a dose-dependent presser effect. The presser response to L-NAME was prevented by pretreatment with L-arginine. Neither D-arginine nor D-NAME modified the MBP. The NO donor sodium nitroprusside (SNP; 0.125 and 0.25 mu mol, i.t.) induced a hypotensive response followed by a presser effect. The dual response to SNP as well as the hypotensive effect of L-arginine were abolished by the guanylate cyclase inhibitor Methylene blue (0.3 mu mol, i.t.). Nicotinic ganglionic blockade by hexamethonium (10 mg/kg, i.v.) reduced the hypotensive effects of both L-arginine and SNP and prevented almost completely the presser effects of either L-NAME or SNP. The presser effect of L-NAME was abolished by 2-amino-5-phosphonovaleric acid (APV; 30 nmol, i.t.), a selective antagonist of glutamate receptors of the NMDA subtype. These results suggest that in the spinal cord of pentobarbital-anesthetized rats NO exerts both inhibitory and excitatory effects on the preganglionic sympathetic nerve activity related to the control of the BP. The synthesis of NO appears to be tonically activated through the stimulation of spinal glutamate receptors of the NMDA subtype. (C) 1997 Elsevier Science B.V.