Nitric oxide (NO) release from endothelial and/or neuronal nitric oxide synthase (NOS) could be modulated by sympathetic nerve activity and contribute to increased blood flow after exercise. We examined the effects of brachial-arterial infusion of the neuronal NOS (nNOS) selective inhibitor, S-methyl-L-thiocitrulline (SMTC), and the non-selective NOS inhibitor, NG-monomethyl-L-arginine (L-NMMA) on forearm arm blood flow at rest, during sympathetic activation by lower body negative pressure, and during lower body negative pressure immediately after handgrip exercise. Reduction in forearm blood flow by lower body negative pressure during infusion of SMTC was not significantly different from that during vehicle (-28.5±4.02 vs -34.1±2.96% respectively, P=0.32, n=8). However, L-NMMA augmented the reduction in forearm blood flow by lower body negative pressure (-44.2±3.53 vs -23.4±5.71%, n=8, P<0.01). When lower body negative pressure was continued after handgrip exercise, there was no significant effect of either L-NMMA or SMTC on forearm blood flow immediately after low intensity (P=0.91 and P=0.44 for L-NMMA vs. saline and SMTC vs saline respectively, each n=10) or high intensity exercise (P=0.46 and P=0.68 for L-NMMA vs. saline and SMTC vs saline respectively, each n=10). These results suggest that sympathetic activation increases NO release from endothelial NOS (eNOS), attenuating vasoconstriction. Dysfunction of eNOS could augment vasoconstrictor and blood pressure responses to sympathetic activation. However, neither eNOS nor nNOS play an essential role in post exercise hyperaemia, even in the presence of increased sympathetic activation.
- endothelial nitric oxide synthase
- forearm blood flow
- neuronal nitric oxide synthase
- sympathetic vasoconstriction
- Copyright © 2012, American Journal of Physiology - Heart and Circulatory Physiology