Modulation of arteriolar sympathetic constriction by local nitric oxide: onset during rapid juvenile growth

The goal of this study was to determine if the endogenous activity of nitric oxide (NO) and/or prostanoids can limit arteriolar responses to increased sympathetic nerve activity in striated muscle, and to explore possible changes in these influences during rapid juvenile growth. Using intravital microscopy, arteriolar responses to 2-16 Hz sympathetic nerve stimulation were studied in the superfused spinotrapezius muscle of weanling (4-5 weeks old) and juvenile (7-8 weeks old) rats. Nerve stimulation elicited frequency-dependent arteriolar constrictions that were abolished in both age groups by the fast Na+-channel blocker tetrodotoxin or the alpha-antagonist phentolamine. Diameter and flow responses to 2-8 Hz stimulation were greater in juvenile rats than in weanling rats. In juvenile rats but not in weanling rats, the NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) reduced arteriolar diameters and blood flow at rest and enhanced the arteriolar diameter and flow responses to sympathetic nerve stimulation. The cyclooxygenase inhibitor meclofenamate reduced resting arteriolar diameters in both age groups, but had no effect on responses to sympathetic nerve stimulation in either group. These results suggest that juvenile growth is accompanied by an overall increase in arteriolar responsiveness to sympathetic nerve activity, and by the onset of local NO activity that limits this increased responsiveness.