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(Hypertension. 2000;36:1089.)
© 2000 American Heart Association, Inc.

Colin Johnston - A Celebration

Nitric Oxide Limits Pressor Responses to Sympathetic Activation in Rat Spinal Cord

Leonard F. Arnolda; Douglas J. McKitrick; Ida J. Llewellyn-Smith; Jane B. Minson

From the Cardiovascular Neuroscience Group, Cardiovascular Medicine and Centre for Neuroscience, Flinders University, SA 5042, Australia.

Correspondence to Assoc Prof Leonard Arnolda, Department of Cardiology, Division of Medicine, Flinders Medical Centre, Bedford Park, South Australia 5042, Australia. E-mail Leonard.Arnolda{at}flinders.edu.au

Abstract—N-methyl D-aspartate (NMDA) receptor stimulation is known to activate nitric oxide (NO) synthase, an enzyme present in a high proportion of sympathetic preganglionic neurons. In this study, we have examined the possibility that NO modulates the pressor responses elicited by NMDA receptor stimulation in the spinal cord. In experiments on anesthetized rats, we determined whether intrathecal administration of either 3-morpholinylsydnoneimine chloride (SIN-1), an NO donor, or N^G-nitro-L-arginine methyl ester (L-NAME), an NO synthase inhibitor, affected the response to stimulation of spinal NMDA receptors by NMDA (1 pmol to 1 µmol in 10-µL intrathecal administration). Intrathecal NMDA resulted in dose-dependent increases in blood pressure. SIN-1 (100 nmol) attenuated the pressor responses to NMDA (F_1,70=12, P=0.001). Conversely, L-NAME (1 nmol to 1 µmol) augmented the pressor response to NMDA in a dose-dependent manner (F_3,161=28.3, P<0.001). The effect of L-NAME to amplify the pressor response to NMDA was reversed by L-arginine but not by D-arginine. These results indicate that endogenous synthesis of NO in the spinal cord limits the pressor response to stimulation of spinal NMDA receptors.

Key Words: blood pressure • sympathetic nervous system • nitric oxide synthase • L-NAME

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