Modulatory role of nitric oxide on angiotensins vasoconstriction

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...

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Bibliographic Details
Published inRomanian journal of physiology : physiological sciences Vol. 33; no. 1-4; p. 83
Main Authors Haulică, I, Todiraş, M, Brăiloiu, E, Bălţatu, O
Format Journal Article
LanguageEnglish
Published Romania 01.01.1996
Subjects
Angiotensin I - drug effects
Angiotensin I - physiology
Angiotensin II - drug effects
Angiotensin II - physiology
Angiotensin-Converting Enzyme Inhibitors - pharmacology
Animals
Aorta - drug effects
Aorta - physiology
Captopril - pharmacology
Enzyme Inhibitors - pharmacology
Male
Muscle, Smooth, Vascular - drug effects
NG-Nitroarginine Methyl Ester - pharmacology
Nifedipine - pharmacology
Nitric Oxide - antagonists & inhibitors
Nitric Oxide - physiology
Rats
Rats, Wistar
Saralasin - pharmacology
Vasoconstriction - drug effects
Vasodilator Agents - pharmacology
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Summary: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.
ISSN:1223-4974