Effects of medullary administration of a nitric oxide precursor on cardiovascular responses and neurotransmission during static exercise following ischemic stroke

Abstract

We have reported that in rats with a 90 min left middle cerebral artery occlusion (MCAO) and 24 h reperfusion, pressor responses during muscle contractions were attenuated, as were glutamate concentrations in the left rostral ventrolateral medulla (RVLM) and left caudal VLM (CVLM), but gamma-aminobutyric acid (GABA) levels increased in left RVLM and CVLM. This study determined the effects of L-arginine, a nitric oxide (NO) precursor, within the RVLM and (or) CVLM on cardiovascular activity and glutamate/GABA levels during static exercise in left-sided MCAO rats. Microdialysis of L-arginine into left RVLM had a greater attenuation of cardiovascular responses, a larger decrease in glutamate, and a significant increase in GABA levels during muscle contractions in stroke rats. Administration of N(G)-monomethyl-L-arginine, an NO-synthase inhibitor, reversed the effects. In contrast, L-arginine administration into left CVLM evoked a greater potentiation of cardiovascular responses, increased glutamate, and decreased GABA levels during contractions in stroked rats. However, L-arginine administration into both left RVLM and left CVLM elicited responses similar to its infusion into the left RVLM. These results suggest that NO within the RVLM and CVLM modulates cardiovascular responses and glutamate/GABA neurotransmission during static exercise following stroke, and that a RVLM-NO mechanism has a dominant effect in the medullary regulation of cardiovascular function.

The S-Nitrosylation Status of PCNA Localized in Cytosol Impacts the Apoptotic Pathway in a Parkinson’s Disease Paradigm

“…Nitric oxide (NO) is a free radical in a highly diffusible gaseous state and is regarded as an important regulator for numerous biological processes, such as vasodilation [ 7 ], neurotransmission [ 8 ], and inflammatory responses [ 9 ]. Excessive production of NO and NO-derivative reactive nitrogen species (RNS) has been implicated in neuron damage, particularly neurodegeneration in PD [ 10 – 12 ].…”

No-Ergic Control of Blood Circulation in the Medulla Oblongata of Rats With Experimental Hemiparkinsonizm Under Exposure to Continuous Light

“…Рівні активності цих ензимів і відповідно продукції оксиду азоту (NO) у довгастому мозку, який традиційно вважається важливим центром регуляції функції кровообігу, ще не з'ясовані. Накопичена величезна кількість даних [5][6][7][8][9], які свідчать про залучення NO у медулярний контроль діяльності серцево-судинної системи як гальмівного трансмітера. У довгастому мозку ідентифіковано велику кількість NOсинтезувальних нейронів [10,11].…”

Downregulation of nitric oxide by electroacupuncture against hypoxic-ischemic brain damage in rats via nuclear factor-κB/neuronal nitric oxide synthase

“…NO is biosynthesized from L-arginine, oxygen and nicotinamide adenine dinucleotide phosphate by various nitric oxide synthase (NOS) enzymes in vivo ( 7 ), including neuronal NO synthase (nNOS), endothelial NO synthase and inducible NO synthase. NO can regulate various biological processes in vertebrates, including the regulation of blood flow ( 8 ), blood flow metabolism coupling ( 9 ), neurotransmission ( 10 ), memory formation ( 11 ) and the prevention of apoptosis in neurons ( 12 ). In particular, NO is involved in regulating hypoxic-ischemic brain damage (HIBD) ( 13 ).…”