Key result
Enalapril pretreatment (30 mg/kg/day i.p. for up to 15 days) increased kidney mitochondrial nitric oxide synthase activity by 5-fold and protein levels by 2.3-fold in rats.
Enalapril increases mitochondrial nitric oxide synthase activity and NO production, which in turn regulates mitochondrial respiration and hydrogen peroxide production.
Hypothesis-generating for ACEI effects on renal mitochondrial NOS; leaves open translation to human kidney disease.
Nitric oxide synthase activity was recognized in rat renal cortex mitochondria (mtNOS) with nitric oxide (NO) production rates of 0.14-0.78 nmol/min/mg of protein. Rat pretreatment with enalapril (30 mg/kg/day i.p., up to 15 days) increased NO production in kidney, liver, and heart mitochondria. In kidney, mtNOS activity and mtNOS protein, measured by western blot densitometry, were 5 and 2.3 times increased, respectively. Electron paramagnetic resonance analysis with the probe N-methyl-D-glucamine dithiocarbamate/FeSO(4) detected NO production in mitochondria isolated from enalapril-treated rats, but not in control untreated animals. Polyclonal antibodies anti-iNOS and anti-nNOS detected kidney mtNOS in western blots and inhibited mtNOS biochemical activity. The enzymatic activity of kidney mtNOS generates intramitochondrial NO concentrations that regulate mitochondrial functions: state 3 respiration was decreased by 12-28%, and state 4 hydrogen peroxide production was increased 12-35%.
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Boveris et al. (2003) studied this question. Enalapril vs. Control untreated animals was evaluated on Kidney mtNOS activity and mtNOS protein. Enalapril pretreatment (30 mg/kg/day i.p. for up to 15 days) increased kidney mitochondrial nitric oxide synthase activity by 5-fold and protein levels by 2.3-fold in rats.
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