Increases in vascular nitrosylation reduce blood pressure in hypertensive rats and are associated with a decrease in angiotensin-converting enzyme tissue activity.

The antihypertensive effects of nitrate and nitrite are widely described. Likewise, the physiological relevance of the nitrate-nitrite-nitric Oxide (NO) cycle in cardiovascular homeostasis is well known. Nevertheless, the mechanisms underlying the effects of nitrite are not completely understood, particularly in relation to S-nitrosothiol formation. On the other hand, the angiotensin-converting enzyme (ACE) plays a central role in blood pressure regulation, and little is known about its interaction with NO. This study focused on gaining a better understanding of the impact of S-nitrosylation over blood pressure, especially on ACE. For this purpose, 2K1C hypertensive rats were treated with nitrite or S-nitrosoglutathione (GSNO), resulting in a reduction of approximately 40% in blood pressure and a significant increase in protein S-nitrosylation in the aorta, as well as in nitrosylated species in plasma. Additionally, a significant decrease in ACE activity in the aorta was observed. Treatment with buthionine sulfoximine (BSO), an inhibitor of glutathione synthesis, abolished the antihypertensive effects of nitrite and prevented the increase in protein S-nitrosylation in the aorta, which was associated with the loss of effects on ACE. These findings support the idea that an increase in S-nitrosylation in the vasculature could participate in the reduction of blood pressure and could reduce ACE activity in the vasculature.