Affiliations 

  • 1 School of Pharmaceutical Sciences, Universiti Sains Malaysia, Penang, Malaysia. raza_chohan487@hotmail.com
  • 2 School of Pharmaceutical Sciences, Universiti Sains Malaysia, Penang, Malaysia. munavvar@usm.my
  • 3 School of Pharmaceutical Sciences, Universiti Sains Malaysia, Penang, Malaysia
  • 4 Department of Physiology, University College Cork, Cork, Ireland
  • 5 Department of Pharmacology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia
J. Physiol. Pharmacol., 2016 Feb;67(1):31-44.
PMID: 27010893

Abstract

The present study investigated the role of endothelial nitric oxide synthase (eNOS) enzyme in the development of left ventricular hypertrophy (LVH) in Wistar-Kyoto rats. The effect of L-arginine administration on cardiac structure, arterial stiffness, renal and systemic hemodynamic parameters was studied and the change in expression of eNOS and cystathione γ lyase (CSE) in the myocardium of LVH rats was evaluated. LVH was induced using isoprenaline (5 mg/kg, S.C.) and caffeine (62 mg/L in drinking water) for 14 days. Following to that, L-arginine (1.25g/L in drinking water) was given for 5 weeks as a donor of NO. eNOS and CSE gene expressions were down regulated in the LVH group by about 35% and 67% respectively when compared to control. However, in the LVH group treated with L-arginine there was up regulation of eNOS by almost 27% and down regulation in CSE by 24% when compared to control (all P < 0.05). Heart index and H2S plasma levels were reduced by almost 53% in the L-arginine treated LVH group compared to the control (all P < 0.05). Mean arterial pressure, heart rate and pulse wave velocity were reduced while renal blood perfusion increased in L-arginine treated LVH rats compared to their untreated counterparts (all P < 0.05). The enhanced expression of eNOS in L-arginine treated LVH rats resulted in the amelioration of oxidative and haemodynamic parameters suggesting that NO system is an important therapeutic target in cardiac and LV hypertrophies.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.

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