Md. Garcia et al., POSSIBLE PARTICIPATION OF SPINAL NITRIC-OXIDE IN THE CONTROL OF THE BLOOD-PRESSURE IN ANESTHETIZED RATS, Brain research, 764(1-2), 1997, pp. 67-74
In pentobarbital-anesthetized rats the intrathecal (i.t.) injection of
the nitric oxide (NO) precursor, L-arginine (10 and 20 mu mol), elici
ted 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 resp
onse to L-NAME was prevented by pretreatment with L-arginine. Neither
D-arginine nor D-NAME modified the MBP. The NO donor sodium nitropruss
ide (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 cycla
se inhibitor Methylene blue (0.3 mu mol, i.t.). Nicotinic ganglionic b
lockade by hexamethonium (10 mg/kg, i.v.) reduced the hypotensive effe
cts of both L-arginine and SNP and prevented almost completely the pre
sser 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 pregangl
ionic sympathetic nerve activity related to the control of the BP. The
synthesis of NO appears to be tonically activated through the stimula
tion of spinal glutamate receptors of the NMDA subtype. (C) 1997 Elsev
ier Science B.V.