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Avocado Oil Improves Renal Vasorelaxation in Hypertensive Rats; Probable Role of Decreased Mitochondrial ROS Generation and Enhanced Antioxidant Capacity
Author(s) -
Paz Jose Lucio Hernandez,
MarquezRamirez Cristian,
AguilarToral Roxana,
MoenoJimenez Mario,
RayaFarias Andres,
SalgadoGarciglia Rafael,
GodinezHernandez Daniel,
SaavedraMolina Alfredo,
CortesRojo Christian
Publication year - 2016
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.30.1_supplement.1100.10
Subject(s) - oxidative stress , reactive oxygen species , kidney , endocrinology , medicine , mitochondrial ros , mitochondrion , antioxidant , chemistry , vasodilation , pharmacology , biochemistry
Kidney disease is a major complication of hypertension. Both mitochondrial dysfunction and increased ROS generation are involved in the exacerbated vasoconstriction observed in rodent models of hypertension in response to the increased activity of angiotensin II. Thus, the prevention of mitochondrial dysfunction along with decreased ROS generation or increased activity of antioxidant systems may improve the response to vasorelaxant and/or vasoconstrictor agents, leading to attenuation of hypertensive kidney damage. An increasing body of evidence indicates that avocado oil (AO) intake improves the mitochondrial function and its redox state in kidney, liver and brain of diabetic rats, which has been attributed to the wide array of lipophilic antioxidants contained in AO. We have observed that avocado oil consumption protects from kidney mitochondrial dysfunction elicited by L‐NAME‐induced hypertension. However, it is unknown whether this might lead to attenuation of oxidative stress because decreased ROS generation and improvement of kidney vasodilator responses. Thus, we aimed to test the effect of AO intake in rats treated with L‐NAME on ROS generation, GSH/GSSG ratio (i.e a marker of oxidative stress) in kidney mitochondria and vasodilator responses to a cholinergic agonist in isolated perfused kidney. ROS generation stimulated by complex I substrates increased twice in L‐NAME treated rats while the addition of antimycin A, a complex III inhibitor, exacerbated this effect, suggesting a role for complex III in ROS overproduction. Despite this, L‐NAME did not modified the GSH/GSSG ratio. L‐NAME rats also exhibited a decline in kidney vasorelaxation induced by carbachol. AO supplementation by 90 days (1mL/250g body weight) inhibited ROS generation by below of the values observed in control rats, increased twice the GSH/GSSG ratio and normalized the vasorelaxation stimulated by carbachol. These results suggest that AO improves renal vasorelaxation in association with a decrease in mitochondrial ROS generation and enhancement of antioxidant capacity. Support or Funding Information Supported by Programa de Investigación 2016 de la Coordinación de la Investigación Científica de la UMSNH (CIC‐UMSNH) (CCR).