Interactions between oxidative stress and inflammation in salt-sensitive hypertension (original) (raw)
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Hypertension, 2005
The goal of this study was to test the hypothesis that oxidative stress in Dahl salt-sensitive (SS) rats on a high-sodium intake contributes to the progression of renal damage, the decreases in renal hemodynamics, and the development of hypertension. We specifically studied whether antioxidant therapy, using vitamins C and E, could help prevent renal damage and glomerular filtration rate (GFR) and renal plasma flow reductions and attenuate the increases in arterial pressure. Thirty-three 7-to 8-week old Dahl SS/Rapp strain rats were placed on either a high-sodium (8%) or a low-sodium (0.3%) diet with or without vitamin E (111 IU/d) in the food and 98 mg/d vitamin C in the drinking water for 5 weeks. Rats were equipped with indwelling arterial and venous catheters at day 21. By day 35 in the rats with high-sodium diet, vitamin C and E treatment significantly decreased renal cortical and medullary O 2 ⅐Ϫ release, mean arterial pressure, urinary protein excretion, glomerular necrosis, and renal tubulointerstitial damage. At this time, GFR significantly decreased in the high-sodium diet group (1.6Ϯ0.2 mL/min) when compared with either the high-sodium plus vitamins C and E (2.9Ϯ0.2 mL/min) or the low-sodium diet group (2.9Ϯ0.3 mL/min). In SS rats on high-sodium diet, renal plasma flow decreased 40%, and this reduced flow was restored by vitamin treatment. In Dahl salt-sensitive hypertension, increased oxidative stress plays an important role in the renal damage, decreases in renal hemodynamics, and increases in arterial pressure that occur. Antioxidant treatment with vitamins C and E improves renal dysfunction, lessens renal injury, and decreases arterial pressure in Dahl salt-sensitive hypertension. (Hypertension. 2005; 45:934-939.
Oxidative Stress and Antioxidant Treatment in Hypertension and the Associated Renal Damage
American Journal of Nephrology, 2005
Reactive oxygen species (ROS) are elevated in humans with hypertension many of which develop end-stage renal disease (ESRD), and antioxidant capacity is decreased. About one-half of essential hypertensives have a salt-sensitive type of hypertension, and the amount of renal damage that occurs in salt-sensitive hypertensives greatly exceeds that of non-salt-sensitive hypertensives. Antioxidant therapy can improve cardiovascular outcomes in humans but only if sufficient doses are used. Salt-sensitive hypertensive animal models, especially Dahl salt-sensitive rats, have been used to investigate the relationship between hypertension, ROS and end-stage renal damage. In experimental salt-sensitive hypertension, ROS increase and significant renal damage occur. In the Dahl salt-sensitive (S) rat on high Na for 3 weeks, renal damage is mild, renal levels of superoxide dismutase are decreased, and treatment with Tempol reduces arterial pressure. In the Dahl S rat on high Na for 5 weeks, renal ...
American Journal of Physiology-Renal Physiology, 2004
Recent evidence indicates that interstitial infiltration of T cells and macrophages plays a role in the pathogenesis of salt-sensitive hypertension. The present review examines this evidence and summarizes the investigations linking the renal accumulation of immune cells and oxidative stress in the development of hypertension. The mechanisms involved in the hypertensive effects of oxidant stress and tubulointerstitial inflammation, in particular intrarenal ANG II activity, are discussed, focusing on their potential for sodium retention. The possibility of autoimmune reactivity in hypertension is raised in the light of the proinflammatory and immunogenic pathways stimulated by the interrelationship between oxidant stress and inflammatory response. Finally, we present some clinical considerations derived from the recognition of this interrelationship.
The role of oxidative stress in salt-induced hypertension
American journal of hypertension, 2004
Impairment of endothelial function during hypertension is associated with increased production of superoxide radicals and reduced antioxidants. We investigated the involvement of oxidative stress in Dahl salt-sensitive (SS) and salt-resistant (SR) rats. For a 2-week period, male rats were fed either high salt (HS; 8% sodium chloride) or low salt (LS; 0.3% sodium chloride) diets. Before and weekly on the diets, mean arterial pressure (MAP) and heart rate were measured by tail-cuff plethysmography. At the end of the experiment, plasma and tissue samples were collected for analysis of nitric oxide, prostacyclin, glutathione, and isoprostane. The MAP was increased in SS rats on HS diet, but not in those on a LS diet or in SR rats on either diet. Plasma levels of nitric oxide were reduced in SS rats on HS diet. Plasma prostacyclin levels in SS rats on either diet were lower than SR on LS diet. Increased dietary salt reduced plasma prostacyclin levels in SR, but not in SS rats. Plasma tot...
2010
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. (Hypertension. 2007;49[part 2]:664-671.)
Hypertension, 2003
Previous studies have demonstrated that oxidative stress contributes to hypertension and treatments with either antioxidant or immunosuppressive/anti-inflammatory agents improve hypertension in spontaneously hypertensive rats (SHR). The present study was performed to determine if the antihypertensive effects of an antioxidant-rich diet are associated with reduction in the renal immune infiltration. Rats were divided into experimental groups (nϭ5 each) that were followed 7 months after birth, during which they were fed either a regular or antioxidant-enriched (test) diet as follows: SHR-R groupϭregular diet; SHR-T groupϭtest diet throughout the experiment; SHR-S groupϭtest diet for 4 months switched to regular diet thereafter; WKY groupϭcontrol rats given regular diet. The SHR-T rats showed a significant reduction in systolic blood pressure (mm Hg): SHR-Tϭ179.6Ϯ12.9 versus SHR-Rϭ207.5Ϯ9.6 (PϽ0.001) and plasma hydrogen peroxide concentration (SHR-Tϭ15Ϯ4 mol/L versus 34Ϯ9 in SHR-R rats). This was accompanied by significant reductions of renal tissue nitrotyrosine abundance, tubulointerstitial infiltration (cells/mm 2 ) of lymphocytes (SHR-Tϭ18Ϯ3 versus SHR-Rϭ30Ϯ4, PϽ0.001), macrophages (SHR-Tϭ 17Ϯ3 versus SHR-Rϭ22Ϯ3), and angiotensin II-positive cells (SHR-Tϭ 17Ϯ2 versus SHR-Rϭ25Ϯ5, PϽ0.01). Results in the SHR-S group were intermediate between the SHR-R and SHR-T groups. The intensity of the infiltration of lymphocytes, macrophages, and angiotensin II-positive cells significantly correlated with systolic blood pressure. Thus, the present study demonstrates that an antioxidant-enriched diet reduces the renal interstitial inflammation and improves hypertension in SHR. These findings point to interrelation between oxidative stress and inflammatory reactivity in the pathogenesis of hypertension. (Hypertension. 2003;41:341-346.)
Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences, 2009
The present study examines whether a long-term high salt diet causes hypertension and renal injury in normal subjects [Sprague-Dawley (SD) rats] and alters renal cytokine-related gene expression profiles. Four 10 week old male SD rats received a high salt diet (HS, 8%) and the other 4 SD rats received a normal salt diet (NS, 0.5%) for 8 weeks. Mean arterial pressure (MAP) and renal damages such as albuminuria and histological renal injury were determined. The relative mRNA levels of 514 cytokine-related genes (normalized by beta-actin) in rat kidneys following NS or HS were determined quantitatively through analysis of 4 sets of gene expression profiles using the mouse cDNA membrane microarrays. We demonstrated that 8 weeks of HS diet increased MAP [(140.0+/-5.3) vs (112.0+/-2.2) mmHg; 1 mmHg=0.133 kPa, P<0.01], albuminuria [(41.4+/-3.2) vs (20.1+/-4.5) mg/d; P<0.01], and caused histological renal injury in SD rats, compared to NS group. Of the 514 genes in the array, there we...
Target for Oxidative Stress in Salt-Sensitive Hypertension
2014
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2016
Abstract—The balance between endothelial nitric oxide (NO) and angiotensin II (Ang II) maintains the homeostasis of the cardiovascular and renal systems. We tested the hypothesis that increased oxidant stress linked to a functional imbalance between NO and Ang II might play a central pathogenetic role in salt-sensitive (SS) hypertension. We studied Dahl SS (DS) rats during the prehypertensive (5 days) and hypertensive (12 weeks) phases of a high-salt (4 % NaCl) diet. Control rats received a normal-salt (0.5 % NaCl, [NS]) diet. Prehypertensive DS rats (systolic blood pressure [SBP] 1382 mm Hg) manifested a 35 % increase (P0.05) in aortic superoxide (O2–) production without evidence of end-organ damage. Hypertensive DS rats (SBP 21411 mm Hg) had impaired endothelium-dependent relaxation (EDR) and increased aortic O2 – production (320%), urinary isoprostane excretion (83%), aortic (20%) and left ventricular (LVH, 21%) hypertrophy, and proteinuria (124%). In prehypertensive DS rats, can...