The inhibition of basal NO synthesis by L-NAME in these
animals could justify these results, but what was more important
in the in vivo experiments in order to corroborate our hypothesis
for the present study was the observed impairment of the CFP antihypertensive effect in the L-NAME treated SHR. Except for some
apparent inconsistencies, it become generally accepted that NO
was the main endothelium derived relaxing factor [21].