Objectives: 

We aimed to establish the role of endothelium on vascular postganglionic sympathetic neural release evaluating NO modulation, per se or combined with other modulators such as adenosine.

Materials: 

Wistar rat (12 weeks-old, 270-360g) artery preparations with and without endothelium (mechanically removed), preincubated with 0.1 &#956;M [3H]-noradrenaline (40 min, at 37ordm;C), were submitted to 3 identical periods of stimulation (5 Hz, 100 pulses, 1 ms, 50 mA) every 20 min (S0-S2). Effects of drugs, such as NO donors (sodium nitroprusside, SNP, and NONOate), selective A2A-adenosine receptor antagonist (SCH 58261), enzyme substrate/inhibitor (L-arginine, L-NAME), on noradrenaline (NA) release (estimated as tritium overflow) were studied. Results are expressed as mean±s.e.m; statistically significant differences (ANOVA followed by Holm-Sidak or Student's t test): *p<0.05 or **p<0.001, from the respective control and #p<0.05 or ##p<0.001, from the endothelium intact artery preparations.

Results: 

In endothelium-intact artery preparations, L-NAME (100mM) inhibited NA release (0.74±0.045%, n=20) while L-arginine (1 mM) and SNP (10mM) facilitated NA release (1.15±0.241%, n=6, **p<0.001 and 1.22±0.04%, n=6, **p<0.001, respectively). Moreover, SCH 58261 did not change NA release (0.97±0.08%, n=25, **p<0.001). However, in endothelium denuded arteries, L-NAME and L-arginine failed to influence NA release (1.03±0.082%, n=17, ##p<0.001 and 0.94±0.167%, n=7, respectively) whereas NO donors, SNP (0.76±0.061%, n=8,**p<0.001; ##p<0.001) or NONOate (0.63±0.036%, n=3,**p<0.001), as well as NBTI (5 mM, a nucleoside transporter inhibitor) and SCH 58261(20 nM) had inhibited NA release up to 30% (0.48±0.058%, n=6,**p<0.001 and 0.66±0.05%, n=6, **p<0.001; ##p<0.001, respectively).

Conclusions: 

Data indicated that endothelial nitric oxide seems to modulate vascular sympathetic noradrenaline release.