Effects of medullary administration of nitric oxide precursor on cardiovascular responses and neurotransmission during static exercise in stroke rats

Abstract

Rats with a 90‐min left middle cerebral artery occlusion followed by 24‐hour reperfusion (MCAO), pressor responses during muscle contractions were attenuated, as were glutamate in the left rostral ventrolateral medulla (RVLM) and left caudal VLM (CVLM), but GABA increased in left RVLM and CVLM (Brain Res. 2002: 952). This study determined the effects of L‐arginine (L‐Arg), a nitric oxide (NO) precursor, within the RVLM or CVLM on cardiovascular activity and glutamate/GABA levels during static exercise in left‐sided MCAO rats. Microdialysis of L‐Arg into the left RVLM further attenuated pressor and heart rate (HR) responses, decreased glutamate and increased GABA levels during muscle contractions. Administration of N(G)‐monomethyl‐L‐arginine, an NO‐synthase inhibitor, reversed the effects. In contrast, L‐Arg administration into left CVLM potentiated pressor and HR responses, increased glutamate and decreased GABA levels during muscle contractions. However, simultaneous L‐Arg microdialysis into left RVLM and CVLM elicited responses similar to those following its infusion into RVLM. Results suggest that NO within the RVLM and CVLM plays an important role in modulating cardiovascular responses and glutamate/GABA neurotransmission during static exercise following stroke, and that the RVLM‐NO mechanism has a dominant effect in medullary regulation of cardiovascular function.