The role of inflammatory markers in the cardioprotective effect of L-carnitine in L-NAME-induced hypertension

Am J Hypertens. 2008 Nov;21(11):1231-7. doi: 10.1038/ajh.2008.271. Epub 2008 Sep 11.


Background: The mechanism(s) underlying the effects of L-carnitine (beta-hydroxy-gamma-N-trimethylammonium-butyrate; LC) in cardiovascular diseases are not well clarified. 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 LC might attenuate the hypertensive status through an inhibition of inflammation process.

Methods: Heart mRNA expression and plasma levels of inflammatory markers, interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha), were measured in rats that were made hypertensive with N(omega)-nitro-L-arginine methyl ester (L-NAME) and subjected to a simultaneous administration of LC. To clarify the role of the renin-angiotensin system (RAS) in this effect of LC, the activity and expression of angiotensin I-converting enzyme (ACE) as well as the expression of angiotensin II type I receptor (AT1R) 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 expression of IL-1 beta, IL-6, and TNF-alpha showed an increase in the L-NAME group, which was reversed by LC treatment. The plasma ACE activity was not modified between normotensive and hypertensive rats although LC treatment produced a reduction of these values in the latter. Finally, protein and mRNA expression of ACE and AT1R was enhanced in the heart of L-NAME-treated animals, and LC reversed these values.

Conclusions: The chronic administration of LC reduces blood pressure and attenuates the inflammatory process associated with arterial hypertension. LC might produce a partial inactivation in the RAS resulting in a reduction in the production and effects of angiotensin II.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Biomarkers / metabolism
  • Blood Pressure / drug effects
  • Blood Pressure / physiology
  • Body Weight / drug effects
  • Body Weight / physiology
  • Cardiotonic Agents / pharmacology*
  • Carnitine / pharmacology*
  • Disease Models, Animal
  • Hypertension / chemically induced
  • Hypertension / metabolism*
  • Interleukin-1beta / metabolism*
  • Interleukin-6 / metabolism*
  • Male
  • Myocardium / metabolism
  • NG-Nitroarginine Methyl Ester / adverse effects*
  • Peptidyl-Dipeptidase A / metabolism
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Wistar
  • Receptor, Angiotensin, Type 1 / metabolism
  • Renin-Angiotensin System / drug effects
  • Renin-Angiotensin System / physiology
  • Tumor Necrosis Factor-alpha / metabolism*


  • Biomarkers
  • Cardiotonic Agents
  • Interleukin-1beta
  • Interleukin-6
  • RNA, Messenger
  • Receptor, Angiotensin, Type 1
  • Tumor Necrosis Factor-alpha
  • Peptidyl-Dipeptidase A
  • Carnitine
  • NG-Nitroarginine Methyl Ester