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Hypertension affects the regulatory effect of nitric oxide on the respiratory chain
Author(s) -
CalderónCortés Elizabeth,
CortésRojo Christian,
ServínCampuzano Luisa,
ClementeGuerrero Mónica,
NoriegaCisneros Ruth,
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.701.1
Subject(s) - mitochondrion , nitric oxide , medicine , endocrinology , respiratory chain , snap , oxidative phosphorylation , kidney , cytochrome c oxidase , chemistry , coenzyme q – cytochrome c reductase , mitochondrial respiratory chain , basal (medicine) , nitric oxide synthase , biology , biochemistry , cytochrome c , computer graphics (images) , computer science , insulin
Nitric oxide (NO) synthesized from mitochondrial nitric oxide synthase (NOSmt) contributes to the regulation of oxidative phosphorylation by inhibiting ATP synthesis through the binding of NO to cytochrome c oxidase complex (complex IV) of the electron transport chain (ETC). We hypothesize that during hypertension the regulation of the ETC exerted by NO could be affected and could lead to a disruption in the mitochondrial energetic metabolism. Basal oxygen consumption during state 3 was increased in liver and kidney mitochondria from SHR of 1 and 7‐m.o. as compared with WKY animals of the same age. The sensitivity of complex IV to SNAP inhibition was lower in liver and kidney mitochondria from 7‐m.o. SHR as compared with mitochondria from WKY animals of the same age. Differential susceptibility to inhibition by SNAP was observed in complex IV activity from SHR rats of 7 months old for both organs. Activity of complex IV was inhibited with SNAP in a concentration‐dependent fashion in both WKY and SHR kidney and liver mitochondria from 1‐m.o. rats. The results suggest that hypertension lead to changes in ETC activity at the level of complex IV, which may be related with assembly defects of this complex during hypertension reported by others and contributes to mitochondrial dysfunction in kidney and liver during hypertension progression.