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Increases in vascular nitrosylation reduce blood pressure in hypertensive rats and are associated with a decrease in

Lucas C Pinheiro1,2, Gustavo H Oliveira-Paula3, Graziele C Ferreira3

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Nitrite treatment lowers blood pressure in hypertensive rats by increasing S-nitrosylation, which reduces angiotensin-converting enzyme (ACE) activity. Glutathione synthesis inhibition blocks these blood pressure-lowering effects.

Keywords:
ACEHypertensionNitriteS-nitrosoglutathioneS-nitrosylation

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Area of Science:

  • Cardiovascular Physiology
  • Biochemistry

Background:

  • Nitrate and nitrite are known for their antihypertensive effects, linked to the nitric oxide (NO) cycle.
  • The precise mechanisms of nitrite's action, especially concerning S-nitrosothiol formation and interaction with angiotensin-converting enzyme (ACE), remain unclear.

Purpose of the Study:

  • To investigate the impact of S-nitrosylation on blood pressure and ACE activity.
  • To elucidate the role of nitrite and S-nitrosylation in regulating blood pressure in hypertension.

Main Methods:

  • Utilized 2K1C hypertensive rat model.
  • Administered nitrite or S-nitrosoglutathione (GSNO) and observed effects on blood pressure, aortic and plasma S-nitrosylation, and aortic ACE activity.
  • Investigated the role of glutathione synthesis using buthionine sulfoximine (BSO).

Main Results:

  • Nitrite and GSNO treatments reduced blood pressure by ~40% and increased S-nitrosylation in the aorta and plasma.
  • A significant decrease in aortic ACE activity was observed following nitrite/GSNO treatment.
  • Inhibition of glutathione synthesis with BSO abolished the antihypertensive effects and prevented changes in S-nitrosylation and ACE activity.

Conclusions:

  • Increased vascular S-nitrosylation contributes to blood pressure reduction.
  • S-nitrosylation may decrease vascular ACE activity, offering a potential therapeutic mechanism for hypertension.