Modulatory role of nitric oxide on angiotensins vasoconstriction.

Abstract

Using aortic rings from male Wistar rats, we studied the influence of nitric oxide (NO) on the vascular reactivity to angiotensins. The inhibition of NO-synthesis by L-NAME produced on both intact and desendothelised rings an augmentation of vascular reactivity to angiotensins. NO inhibition did not affect the blocking effects of Saralasin to angiotensins vasoconstriction, suggesting that NO cannot act directly on angiotensin II receptor. Nifedipin inhibited the stimulatory effect of L-NAME on angiotensins vasoconstriction. The results of our study provide functional evidence that NO production can interfere with vascular RAS at two levels: 1. by modulating the activity of Ang II-forming enzymes; 2. at intracellular level, by modulating the concentration of calcium. Also, our results suggest the existence of an alternative pathway on Ang II formation, that become more evident with removal of endothelium.