Aim: 

Previous studies have demonstrated that oxidative stress and inflammation contribute to arterial hypertension, and antioxidant and/or anti-inflammatory therapies have been proposed. We hypothesized that L-carnitine (LC), an amino acidic compound used in cardiovascular diseases, might attenuate the hypertensive status through an inhibition of inflammation process.

Methods: 

Heart mRNA expression and plasma levels of inflammatory markers, namely interleukin-1b (IL-1b), interleukin-6 (IL-6) and tumour necrosis factor a (TNF-a), were measured in rats made hypertensive with N^w-nitro-L-arginine methyl ester (L-NAME), which were subjected to a simultaneous chronic administration of LC. Superoxide production via NADPH oxidase expression, angiotensin I converting enzyme (ACE) activity and expression, and angiotensin II type I receptor (AT1R) expression in the heart were also determined.

Results: 

LC produced a significant but not complete reduction of blood pressure in L-NAME-treated rats. Plasma levels and heart mRNA expression of IL-1b, IL-6 and TNF-a showed an increase in the L-NAME group, which was reversed by LC treatment. Plasma ACE activity was not modified between normotensive and hypertensive rats, although LC treatment produced a reduction of this value in the latter. Finally, mRNA expression of p22phox (subunit of NADPH oxidase), ACE and AT1R was enhanced in the heart of L-NAME treated animals, and LC prevented these values.

Conclusion: 

The chronic administration of LC reduces blood pressure and produces a partial inactivation of the renin-angiotensin system that in turn inactivates NADPH oxidase, thus protecting the heart from the inflammatory process associated to arterial hypertension.