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Renin‐angiotensin system involvement in the generation of reactive oxygen and nitrogen species in kidney mitochondria in hypertension
Author(s) -
LópezCastillo Lilia,
GodínezHernández Daniel,
ManzoAvalos Salvador,
UrquizaMarín Héctor,
SaavedraMolina Alfredo
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.665.3
Subject(s) - endocrinology , medicine , captopril , kidney , chemistry , nitric oxide , angiotensin ii , nitric oxide synthase , reactive oxygen species , renin–angiotensin system , mitochondrion , enos , blood urea nitrogen , blood pressure , biology , biochemistry
In maintaining blood pressure (BP) various vasoactive substances are in equilibrium. Nitric oxide (NO) and angiotensin II (Ang ll) play a key role in controlling the BP. The NO and Ang II are regulated each other to maintain adequate Ca 2+ concentrations within the cell. Hypertension (HP) is a consequence of alterations in these mechanisms. HP presents a polygenic and multifactorial etiology yet to be defined completely. Studies found an increase production of reactive oxygen species (ROS), which uncoupled the endothelial nitric oxide synthase (eNOS) activity. In this work we analyze the effect of HP induced by L‐NAME (competitive inhibitor of NOS), in normotensive rats, inhibition of Ang II synthesis with captopril (an inhibitor of angiotensin converting enzyme (ACE) in normotensive and hypertensive rats, ACE inhibition with captopril, measuring the levels of AT 1 receptor expression in the kidney, as well as the different mitochondrial parameters such as NO synthesis (mtNO), oxygen consumption and H 2 O 2 production. Renal damage results measured as creatinine, urea, proteinuria has no changes during the time of HP induction. Mitochondrial NO synthesis diminished 36% in the hypertensive rats group, while had no changes in the other groups. Results of state 3 and 4 of mitochondrial respiration were increased 1.5‐fold and 2‐fold, respectively in the hypertensive rats group, and no change were detected in the other groups. The results suggest that mtNO exerted a crucial effect on rat kidney mitochondria in hypertension.