ROS Production Is Increased in the Kidney but Not in the Brain of Dahl Rats With Salt Hypertension Elicited in Adulthood

Vokurková, M.; Rauchová, Hana; Rezacova, Lenka; Vaněčková, Ivana; Zicha, Josef

doi:10.33549/physiolres.933054

Cited by 8 publications

(3 citation statements)

References 55 publications

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“…Reactive oxygen species such as superoxide (O 2 − ) and hydrogen peroxide (H 2 O 2 ) are increased in the renal cortex in genetic models of salt-sensitive hypertension. 17 HS diet has also been shown to increase 8-isoprostane excretion, a marker for increased renal reactive oxygen species formation. 18 Besides having intrinsic vasoconstrictor properties and decreasing the bioavailability of the intrinsic vasodilator and natriuretic nitric oxide, 19 , 20 it has been reported that reactive oxygen species can stimulate the secretion of renin 21 directly from the juxtaglomerular cells.…”

Section: Introductionmentioning

confidence: 99%

Free radical scavenging reverses fructose-induced salt-sensitive hypertension

Zenner¹,

Gordish²,

Beierwaltes³

2017

IBPC

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We have previously reported that a moderate dietary supplementation of 20% fructose but not glucose leads to a salt-sensitive hypertension related to increased proximal sodium–hydrogen exchanger activity and increased renal sodium retention. We also found that while high salt increased renal nitric oxide formation, this was retarded in the presence of fructose intake. We hypothesized that at least part of the pathway leading to fructose-induced salt-sensitive hypertension could be due to fructose-induced formation of reactive oxygen species and inappropriate stimulation of renin secretion, all of which would contribute to an increase in blood pressure. We found that both 20% fructose intake and a high-salt diet stimulated 8-isoprostane excretion. The superoxide dismutase (SOD) mimetic tempol significantly reduced this elevated excretion. Next, we placed rats on a high-salt diet (4%) for 1 week in combination with normal rat chow or 20% fructose with or without chronic tempol administration. A fructose plus high-salt diet induced a rapid increase (15 mmHg) in systolic blood pressure and reversed high salt suppression of plasma renin activity. Tempol treatment reversed the pressor response and restored high salt suppression of renin. We conclude that fructose-induced salt-sensitive hypertension is driven by increased renal reactive oxygen species formation associated with salt retention and an enhanced renin–angiotensin system.

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Section: Introductionmentioning

confidence: 99%

Free radical scavenging reverses fructose-induced salt-sensitive hypertension

Zenner¹,

Gordish²,

Beierwaltes³

2017

IBPC

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“…The notion in favor of a contributing role of brain mitochondrial dysfunction and ROS accumulation in the pathogenesis of neurogenic hypertension is based on findings that defected mitochondrial biogenesis/bioenergetics and/or increase in tissue ROS levels in brain sites involved REVIEW PHYSIOLOGY • Volume 32 • July 2017 • www.physiologyonline.org in cardiovascular regulation can be detected in pre-hypertensive SHR (25) or before the onset of hypertension induced by central or peripheral Ang II application (159,174). Moreover, no sign of enhanced oxidative stress is detected in the brain of adult Dahl-sensitive hypertensive rats (154). Deletion of brain antioxidants markedly sensitizes Ang II-induced hypertension (18) or enhances the hypertensive response to a low dose of Ang II that usually exerts minimal effect on blood pressure (95).…”

Section: Which Comes First Mitochondrial Dysfunction/ros Generation or Hypertension?mentioning

confidence: 99%

Mitochondria and Reactive Oxygen Species Contribute to Neurogenic Hypertension

Chan

2017

Physiology

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Beyond its primary role as fuel generators, mitochondria are engaged in a variety of cellular processes, including redox homeostasis. Mitochondrial dysfunction, therefore, may have a profound impact on high-energy-demanding organs such as the brain. Here, we review the roles of mitochondrial biogenesis and bioenergetics, and their associated signaling in cellular redox homeostasis, and illustrate their contributions to the oxidative stress-related neural mechanism of hypertension, focusing on specific brain areas that are involved in the generation or modulation of sympathetic outflows to the cardiovascular system. We also highlight future challenges of research on mitochondrial physiology and pathophysiology.

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“…This was a reason why we decided to test the above hypothesis proposed by Fujita (2014) in this hypertensive model. Salt hypertensive Dahl rats are characterized by sympathoexcitation of central origin (Mark 1991, Huang and Leenen 1998, Zicha et al 2001 as well as by numerous renal abnormalities (Alvarez-Guerra et al 2002, Aoi et al 2004, Amin et al 2011, Nishimoto and Fujita 2015, Vokurková et al 2015, Pavlov and Starushenko 2017, Kittikulsuth et al 2018. Thus, we could expect increased β-adrenergic suppression of renal WNK4 pathway which could be prevented by chronic β-adrenergic blockade with non-selective β-blocker propranolol.…”

Section: Introductionmentioning

confidence: 98%

Is Renal β-Adrenergic-WNK4-NCC Pathway Important in Salt Hypertension of Dahl Rats?

Zicha

Hojná²,

Vaňourková³

et al. 2019

Physiol Res

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In 2011 Fujita and coworkers proposed that β-adrenergic stimulation causes decreased serine/threonine-protein kinase WNK4 transcription leading to the activation of Na-Cl cotransporter (NCC) which participates in salt sensitivity and salt hypertension development in rodents. The aim of our study was to investigate whether the above hypothesis is also valid for salt hypertension of Dahl rats, which are characterized by high sympathetic tone and abnormal renal sodium handling. Male 8-week-old salt-sensitive (SS/Jr) and salt-resistant (SR/Jr) Dahl rats were fed either low-salt diet (LS, 0.4 % NaCl) or high-salt diet (HS, 4 % NaCl) for 6 weeks. Half of the animals on either diet were chronically treated with non-selective β-blocker propranolol (100 mg/kg/day). At the end of the experiment diuresis and sodium excretion were measured prior and after hydrochlorothiazide injection (HCTZ, 10 mg/kg i.p.). Furthermore, blood pressure (BP), heart rate (HR), sympathetic (pentolinium 5 mg/kg i.v.) and NO-dependent (L-NAME 30 mg/kg i.v.) BP components were determined. Chronic HS diet feeding increased BP through sympathoexcitation in SS/Jr but not in SR/Jr rats. Concomitant propranolol treatment did not lower BP in either experimental group. Under the conditions of low salt intake HCTZ increased diuresis, natriuresis and fractional sodium excretion in SR/Jr but not in SS/Jr rats. HS diet feeding attenuated renal response to HCT in SR/Jr rats, whereas no HCTZ effect was observed in SS/Jr rats fed HS diet. Propranolol treatment did not modify diuresis or natriuresis in any experimental group. In conclusions, our present data do not support the idea on the essential importance of renal β-adrenergic-WNK4-NCC pathway in pathogenesis and/or maintenance of salt hypertension in Dahl rats. Key words Sympathetic nervous system • β-adrenergic blockade • Renal sodium excretion • NCC cotransporter • Hydrochlorothiazide • Serine/threonine-protein kinase WNK4

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ROS Production Is Increased in the Kidney but Not in the Brain of Dahl Rats With Salt Hypertension Elicited in Adulthood

Cited by 8 publications

References 55 publications

Free radical scavenging reverses fructose-induced salt-sensitive hypertension

Free radical scavenging reverses fructose-induced salt-sensitive hypertension

Mitochondria and Reactive Oxygen Species Contribute to Neurogenic Hypertension

Is Renal β-Adrenergic-WNK4-NCC Pathway Important in Salt Hypertension of Dahl Rats?

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