ArticleAmerican journal of hypertension2011
Introgression of the Brown Norway renin allele onto the Dahl salt-sensitive genetic background increases Cu/Zn SOD expression in cerebral arteries.
Article in American journal of hypertension, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 19 citations in OpenAlex.
- Effect of Chronically Suppressed Plasma Angiotensin II on Regulation of the CYP4A/20-HETE Pathway in the Dahl Salt-Sensitive Rat.Antioxidants (Basel, Switzerland) · 2023Article
- Role of vascular reactive oxygen species in regulating cytochrome P450-4A enzyme expression in Dahl salt-sensitive rats.Microcirculation (New York, N.Y. : 1994) · 2016Article
- Enhancement of resting-state fcMRI networks by prior sensory stimulation.Brain connectivity · 2014Article
- Vascular dysfunction precedes hypertension associated with a blood pressure locus on rat chromosome 12.American journal of physiology. Heart and circulatory physiology · 2014Article
- Amelioration of salt-induced vascular dysfunction in mesenteric arteries of Dahl salt-sensitive rats by missense mutation of extracellular superoxide dismutase.American journal of physiology. Heart and circulatory physiology · 2014Article
- AT1 receptors prevent salt-induced vascular dysfunction in isolated middle cerebral arteries of 2 kidney-1 clip hypertensive rats.American journal of hypertension · 2013Article
- Reduced angiotensin II levels cause generalized vascular dysfunction via oxidant stress in hamster cheek pouch arterioles.Microvascular research · 2013Article
- Low-dose angiotensin II infusion restores vascular function in cerebral arteries of high salt-fed rats by increasing copper/zinc superoxide dimutase expression.American journal of hypertension · 2013Article
- Role of the CYP4A/20-HETE pathway in vascular dysfunction of the Dahl salt-sensitive rat.Clinical science (London, England : 1979) · 2013Review
- Introgression of Brown Norway CYP4A genes on to the Dahl salt-sensitive background restores vascular function in SS-5(BN) consomic rats.Clinical science (London, England : 1979) · 2013Article
- Short-term hypercaloric diet induces blunted aortic vasoconstriction and enhanced vasorelaxation via increased nitric oxide synthase 3 activity and expression in Dahl salt-sensitive rats.Acta physiologica (Oxford, England) · 2013Article
- Dahl salt-sensitive rats are protected against vascular defects related to diet-induced obesity.Hypertension (Dallas, Tex. : 1979) · 2012Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundNitric oxide (NO)-dependent vasodilation is impaired in middle cerebral arteries (MCAs) from Dahl salt-sensitive (SS) rats that are fed normal salt (NS) diet, due to low plasma renin activity and chronic exposure to low plasma angiotensin II (ANG II) levels. NO-dependent vasodilator responses are rescued in MCAs from Ren1-BN congenic rats, which have a 2.0 Mbp portion of Brown Norway (BN) chromosome 13 containing the renin gene introgressed onto the Dahl SS genetic background.
methodsVascular superoxide levels were measured with dihydroethidium (DHE) fluorescence in basilar arteries from 10- to 14-week-old, male Dahl SS and Ren1-BN congenic rats that fed NS diet. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and xanthine oxidase (XO) activity were also measured in cerebral artery tissue homogenates. Expression of the superoxide dismutase (SOD) enzymes was evaluated via western blotting in cerebral arteries from the two rat strains.
resultsSuperoxide levels were significantly higher in basilar arteries from Dahl SS rats compared to Ren1-BN congenic rats. NADPH oxidase and XO activity were similar between the two rat strains. Cu/Zn SOD expression was significantly higher in cerebral arteries from Ren1-BN congenic rats vs. those from Dahl SS rats. The expression of Mn-SOD was similar in cerebral arteries from both strains.
conclusionsThese findings suggest that introgressing the BN renin allele onto the Dahl SS genetic background to restore normal activity of the renin-angiotensin system (RAS) protects NO-dependent vascular relaxation in cerebral arteries by increasing the expression of Cu/Zn SOD and lowering vascular superoxide levels.
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