Currently, nitrate is considered a source of NO. The nitrite may be converted to nitric oxide by enzymatic or chemical means. Works have demonstrated the antihypertensive effect of sodium nitrite in a model of hypertension 2 kidneys 1 clip (2K1C). However, the mechanisms responsible for the antihypertensive effect of nitrite were not fully elucidated. 2K1C hypertension occurs with a significant increase in the angiotensin-converting enzyme (ACE) activity. Since this enzyme is inhibited by NO, we believe that nitrite can inhibit ACE when converted to NO. To prove our hypothesis, we will evaluate whether treatment with sodium nitrite reduces blood pressure increases which are induced by intravenous infusion of angiotensin I and angiotensin II as well as the hypotensive responses to the infusion of bradykinin, indicating potential changes in the activity of ACE alive. Also, we will determine in plasma and aorta the ACE activity and plasma concentrations of nitrite nitrate aiming to correlate it with their activities of ACE.
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