Renal and vascular oxidative stress and salt‐sensitivity of arterial pressure

Manning, R. Davis; Meng, Shumei; Tian, Niu

doi:10.1046/j.0001-6772.2003.01204.x

Cited by 116 publications

(97 citation statements)

References 34 publications

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“…The pathophysiologic mechanisms underlying the development and maintenance of DOCA-salt hypertension include increased levels of arginine vasopressin [120], angiotensin-II/aldosterone [300,313], endothelin [179,204,258,302] and oxidative stress [154,175], excessive activation of the sympathetic nervous system [132] and nitric oxide synthase (NOS) uncoupling due to oxidative depletion of its cofactor tetrahydrobiopterin (BH4) [274]. Indeed, both inhibition of the angiotensin-aldosterone system and endothelin receptor blockade have been shown to prevent cardiac remodeling, even without concomitantly reducing arterial blood pressure [89,257].…”

Section: Doca-salt Ratsmentioning

confidence: 99%

Rodent models of heart failure: an updated review

et al. 2012

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Heart failure (HF) is one of the major health and economic burdens worldwide, and its prevalence is continuously increasing. The study of HF requires reliable animal models to study the chronic changes and pharmacologic interventions in myocardial structure and function and to follow its progression toward HF. Indeed, during the past 40 years, basic and translational scientists have used small animal models to understand the pathophysiology of HF and find more efficient ways of preventing and managing patients suffering from congestive HF (CHF). Each species and each animal model has advantages and disadvantages, and the choice of one model over another should take them into account for a good experimental design. The aim of this review is to describe and highlight the advantages and drawbacks of some commonly used HF rodents models, including both non-genetically and genetically engineered models, with a specific subchapter concerning diastolic HF models.

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Section: Doca-salt Ratsmentioning

confidence: 99%

Rodent models of heart failure: an updated review

et al. 2012

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“…27,28 Kidney damage in DOCA-salt rats is accompanied by a significant increase in the production of reactive oxygen species, proinflammatory cytokines and profibrotic factors. 29 In this study, we investigated the renoprotective effects of cilnidipine in DOCA-salt rats and compared the effects with those of amlodipine. In addition, we also examined the effects of cilnidipine on the renal renin-angiotensin-aldosterone system.…”

Section: Introductionmentioning

confidence: 99%

L/N-type calcium channel blocker cilnidipine ameliorates proteinuria and inhibits the renal renin–angiotensin–aldosterone system in deoxycorticosterone acetate-salt hypertensive rats

et al. 2011

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Cilnidipine, an N/L-type calcium channel blocker, has been reported to inhibit sympathetic nerve activity and has a greater renoprotective effect than L-type calcium channel blockers. To investigate the hypothesis that cilnidipine might ameliorate advanced hypertensive nephropathy and inhibit the renal renin-angiotensin-aldosterone system, cilnidipine (1 mg per kg per day) or amlodipine (1 mg per kg per day) was administered to uninephrectomized deoxycorticosterone (DOCA)-salt hypertensive rats (DOCA-salt) for 4 weeks by gavage. Although the blood pressure in the DOCA-salt group was higher than that of control, neither cilnidipine nor amlodipine had any effect on the increase in blood pressure in the DOCA-salt group. The DOCA (40 mg per kg per week, subcutaneously (s.c.)) and salt (1% NaCl in drinking water) treatment significantly aggravated the levels of urinary protein excretion and creatinine clearance and increased glomerulosclerosis and collagen deposition in the tubulointerstitial area of the kidney. These effects were attenuated by cilnidipine treatment. Reverse transcription-polymerase chain reaction analysis revealed that the renal expression of mRNA for collagen I/IV and transforming growth factor-b was enhanced in the DOCA-salt group and that the overexpression of these molecules was suppressed by cilnidipine. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-derived superoxide production in the kidney and urinary norepinephrine excretion, which were enhanced in the DOCA-salt group, were suppressed by cilnidipine. Cilnidipine also decreased the activity and expression of angiotensin-converting enzyme (ACE) and the aldosterone concentration in the renal homogenate. Although neither cilnidipine nor amlodipine had any effect on the increased blood pressure in the DOCA-salt group, these renal changes were not induced by treatment with amlodipine. In conclusion, cilnidipine inhibited renal dysfunction, sympathetic nerve activity and renal renin-angiotensin-aldosterone system in the DOCA-salt group.

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“…3,13,14 A variety of evidence suggests that reactive oxygen species contribute to impaired endothelial function in several forms of hypertension and that there is increased oxidative stress in the microvessels of spontaneously hypertensive rats and Dahl salt-sensitive hypertensive rats. [15][16][17] A recent report by Lenda et al 7 has suggested that reactive oxygen species can also contribute to a reduced endothelium-dependent dilation in normotensive rats on a high-salt diet. Despite the potential importance of reactive oxygen species in contributing to impaired endothelium-dependent vasodilation and reduced NO production during elevated dietary salt intake, the nature and mechanisms of the impaired vascular relaxation with the high-salt diet and the role of enhanced oxidative stress in contributing to salt-induced changes in vascular function and hypertension are not completely understood.…”

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confidence: 99%

Mechanisms of Oxidative Stress-Induced Increase in Salt Sensitivity and Development of Hypertension in Sprague-Dawley Rats

et al. 2007

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Abstract-High salt intake produces vascular changes that contribute to the development of hypertension in salt-sensitive individuals. Because reactive oxygen species play a role in the pathogenesis of cardiovascular diseases, we investigated whether oxidative stress contributes to salt-sensitive hypertension. Sprague-Dawley rats were divided in different groups and received tap water (vehicle), 30 mmol/L of L-buthionine sulfoximine ([BSO] an oxidant), high salt ([HS] 1% NaCl), and BSO plus HS without and with antioxidant tempol (1 mmol/L) in drinking water for 12 days. Compared with vehicle, BSO treatment caused oxidative stress and mild increase in blood pressure. Thoracic aortic rings from BSO-treated rats exhibited decreased response to endothelium-independent vasorelaxants. In HS-treated rats, the response to vasoactive agents, as well as blood pressure, was unaffected. Concomitant treatment of rats with BSO and HS produced a marked increase in blood pressure and a decreased response to both endothelium-dependent and endothelium-independent vasorelaxants with an increase in EC 50 . Incubation of aortic tissue from BSO-treated rats with sodium nitroprusside showed decreased cGMP accumulation, whereas HS rats had decreased basal NO synthase activity. Tempol decreased oxidative stress, normalized blood pressure, and restored NO signaling and responses to vasoactive compounds in BSO and BSO plus HS rats. We conclude that BSO increases oxidative stress and reduces NO signaling, whereas HS reduces NO levels by decreasing the NO synthase activity. These phenomena collectively result in reduced responsiveness to both endothelium -dependent and endothelium-independent vasorelaxants and may contribute to salt-sensitive hypertension. Key Words: acetylcholine Ⅲ hypertension Ⅲ oxidative stress Ⅲ salt sensitivity Ⅲ tempol E ndothelial cells modulate the reactivity of the underlying vascular smooth muscle cells by releasing endotheliumderived relaxing factors. 1,2 Previous studies have demonstrated that elevated dietary salt intake leads to an impaired relaxation of blood vessels to endothelium-dependent relaxations induced by a variety of vasodilator agents. 3-9 A possible contributor to impaired vascular relaxation to dilator stimuli in animals on a high-salt diet is an impaired function of the endothelium. 3-9 Impaired endothelium-dependent dilation in vessels of animals on a high-salt diet could occur either because the acetylcholine (Ach)-mediated production of NO by the endothelium is impaired or because of the failure of NO to cause vasodilation. [3][4][5][6][7][8][9] NO is a major regulator of vascular tone in humans. 10 Decreased production or bioavailability, or decreased vascular response to NO, has been implicated in the pathogenesis of human hypertension. 11,12 An increase in blood pressure (BP) in response to dietary sodium (salt sensitivity) is a well-documented phenomenon in humans and is considered to be an important factor in the pathogenesis of hypertension. 4 In animal models of salt-sensitive hypertens...

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Renal and vascular oxidative stress and salt‐sensitivity of arterial pressure

Cited by 116 publications

References 34 publications

Rodent models of heart failure: an updated review

Rodent models of heart failure: an updated review

L/N-type calcium channel blocker cilnidipine ameliorates proteinuria and inhibits the renal renin–angiotensin–aldosterone system in deoxycorticosterone acetate-salt hypertensive rats

Mechanisms of Oxidative Stress-Induced Increase in Salt Sensitivity and Development of Hypertension in Sprague-Dawley Rats

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