Oxidative Stress in the Dahl Hypertensive Rat

Swei, Allen; Lacy, Fred; DeLano, Frank A.; Schmid‐Schönbein, Geert W.

doi:10.1161/01.hyp.30.6.1628

Cited by 203 publications

(144 citation statements)

References 26 publications

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“…Oxidative stress develops when the well-regulated balance between prooxidants and antioxidants becomes uncontrolled and tips in favor of pro-oxidants. Oxidative stress is a major contributor to the aging process (26) and appears to be a common feature of hypertensive disorders from diverse origins (9,(27)(28)(29). ROS have also been shown to be involved in cardiac hypertrophy induced by several stimuli, such as mechanical stretch, endothelin and angiotensin II (30).…”

Section: Discussionmentioning

confidence: 99%

Is Cardiac Hypertrophy in Spontaneously Hypertensive Rats the Cause or the Consequence of Oxidative Stress?

et al. 2008

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The aim of this work was to assess the possible correlation between oxidative damage and the development of cardiac hypertrophy in heart tissue from young (40-d-old) and older (4-, 11-and 19-month-old) spontaneously hypertensive rats (SHR) in comparison with age-matched Wistar (W) rats. To this end, levels of thiobarbituric acid reactive substances (TBARS), nitrotyrosine contents, NAD(P)H oxidase activity, superoxide production, and the activities of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were determined. Compared to age-matched normotensive rats, SHR showed a significant increase in systolic blood pressure from 40 d of age and left ventricular hypertrophy (LVH) was significantly evident from 4 months of age. W rats (11-and 19-month-old) also showed an increase in LVH with aging. TBARS and nitrotyrosine levels were similar in young rats from both strains and were significantly increased with age in both strains, with the values in SHR being significantly higher than those in age-matched W rats. NAD(P)H activity was similar in young SHR and W rats, whereas it was higher in aged SHR compared with age-matched W rats. Compared to W rats, superoxide production was higher in aged SHR, and was abolished by NAD(P)H inhibition with apocynin. CAT activity was increased in the hearts of 4-month-old SHR compared to age-matched W rats and was decreased in the hearts of the oldest SHR compared to the oldest W rats. SOD and GPx activities decreased in both rat strains with aging. Moreover, an increase in collagen deposition with aging was evident in both rat strains. Taken together, these data showed that aged SHR exhibited higher cardiac hypertrophy and oxidative damage compared to W rats, indicating that the two undesirable effects are associated. That is, oxidative stress appears to be a cause and/or consequence of hypertrophy development in this animal model. (Hypertens Res 2008; 31: 1465-1476)

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Section: Discussionmentioning

confidence: 99%

Is Cardiac Hypertrophy in Spontaneously Hypertensive Rats the Cause or the Consequence of Oxidative Stress?

et al. 2008

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“…25 Superoxide anion may contribute to increased degradation of nitric oxide, resulting in increased vascular tone. 26,27 Scavenging superoxide by exogenous superoxide dismutase has been reported to result in a fall of blood pressure in SHR but not in WKY. 28 In the present study, the sodium-induced changes in kidney XO activity in Dahl S rats were not dose-dependent.…”

Section: Discussionmentioning

confidence: 99%

Increased Kidney Xanthine Oxidoreductase Activity in Salt-Induced Experimental Hypertension

et al. 1998

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Abstract-Clinical and experimental studies have established an association between high sodium intake and arterial hypertension. The renal mechanisms resulting in impaired sodium excretion in hypertension-prone subjects are not clear. In hypertension-prone rats, high blood pressure results in increased renal mass and hemodynamic changes, both of which may alter renal oxygen distribution. Xanthine oxidoreductase (XOR) oxidizes ATP metabolites hypoxanthine and xanthine to urate. Because XOR is induced by hypoxia, we assessed kidney XOR activity in 2 models of salt-sensitive hypertension, spontaneously hypertensive rats (SHR) and Dahl salt-sensitive (Dahl S) rats. Increasing sodium intake from basal (0.08%) to high (2.56% wt/dry wt in the diet) increased renal XOR activity dose-dependently from 68Ϯ8 to 143Ϯ21 U/mg protein in the Dahl S (PϽ0.05) but not in Dahl salt-resistant (Dahl R) rats. On basal and high sodium diets, SHR had higher renal XOR activity (101Ϯ10 and 134Ϯ26 U/mg protein, respectively) than normotensive Wistar-Kyoto rats (55Ϯ2 and 58Ϯ6 U/mg protein, PϽ0.05). Sodium restriction (0.02% wt/wt) downregulated kidney XOR activity in both Dahl S and R rats by nearly 40%. In SHR, allopurinol treatment totally inhibited renal XOR activity, but neither systolic blood pressure nor renal mass changed. The results suggest that renal XOR induction is a consequence of increased salt intake or the resulting hypertension. However, further studies on renal XOR activity during the development of hypertension are needed to assess the importance of XOR in the pathophysiology of arterial hypertension. (Hypertension. 1998;32:902-906.)Key Words: hypertension, essential Ⅲ xanthine oxidoreductase Ⅲ rats, inbred SHR Ⅲ rats, Dahl Ⅲ hypertrophy Ⅲ sodium Ⅲ allopurinol I n salt-sensitive rats, increasing salt intake results in marked hypertension and left ventricular and renal enlargement within weeks. The genetically related salt-insensitive rats develop these harmful, sodium-induced effects to a much lesser extent.1-3 Kidney transplants derived from normotensive rats have been shown to decrease permanently the systolic blood pressure of an adult salt-sensitive recipient and also abolish the predisposition to hypertension in young animals.4,5 These observations, based on studies on the spontaneously hypertensive rat (SHR) and its normotensive control Wistar-Kyoto rat (WKY) as well as the Dahl saltsensitive (Dahl S) and salt-resistant (Dahl R) rat, indicate the crucial importance of the kidney in the pathogenesis of hypertension. Mechanisms resulting in an impaired excretion of sodium in relation to renal perfusion pressure in saltsensitive rat strains have not been fully worked out.

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“…1,2 The production of superoxide anions in aortic vessels is increased in spontaneously hypertensive rats (SHR). [3][4][5][6] In addition, the production of superoxide anions is increased in deoxycorticosterone acetate-salt hypertensive rats, 4 Dahl-salt hypertensive rats, 7 and stroke-prone SHR (SHRSP). 1,8 Inhibition of ROS reduces blood pressure in SHR.…”

mentioning

confidence: 99%

Increased Reactive Oxygen Species in Rostral Ventrolateral Medulla Contribute to Neural Mechanisms of Hypertension in Stroke-Prone Spontaneously Hypertensive Rats

et al. 2004

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Background-Oxidative stress increases in hypertension. The aim of this study was to determine whether reactive oxygen species (ROS) are increased in the rostral ventrolateral medulla (RVLM) in the brainstem, where the vasomotor center is located, in stroke-prone spontaneously hypertensive rats (SHRSP), and, if so, to determine whether the increased ROS contribute to neural mechanisms of hypertension in SHRSP. Methods and Results-We measured ROS levels in the RVLM of SHRSP and compared them with those in Wistar-Kyoto rats (WKY). Thiobarbituric acid-reactive substances were increased in SHRSP compared with WKY. ROS were measured by electron spin resonance (ESR) spectroscopy. The ESR signal decay rate in the RVLM of SHRSP was significantly increased compared with that in WKY, and this increase was abolished by dimethylthiourea (a hydroxyl radical scavenger). The increased ESR signal decay rate was reduced to the same extent in the presence of desferrioxamine, catalase, and Tiron, indicating that hydroxyl radicals are derived from superoxide anions and hydrogen peroxide. In addition, total superoxide dismutase (SOD) activity in the RVLM was decreased in SHRSP compared with WKY. Furthermore, bilateral microinjection of tempol into the RVLM decreased blood pressure in SHRSP but not in WKY, and MnSOD overexpression in the RVLM of SHRSP decreased blood pressure and inhibited sympathetic nerve activity. Conclusions-These results suggest that superoxide anions in the RVLM, which generate hydroxyl radicals, are increased in SHRSP and contribute to the neural mechanisms of hypertension in SHRSP.

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Oxidative Stress in the Dahl Hypertensive Rat

Cited by 203 publications

References 26 publications

Is Cardiac Hypertrophy in Spontaneously Hypertensive Rats the Cause or the Consequence of Oxidative Stress?

Is Cardiac Hypertrophy in Spontaneously Hypertensive Rats the Cause or the Consequence of Oxidative Stress?

Increased Kidney Xanthine Oxidoreductase Activity in Salt-Induced Experimental Hypertension

Increased Reactive Oxygen Species in Rostral Ventrolateral Medulla Contribute to Neural Mechanisms of Hypertension in Stroke-Prone Spontaneously Hypertensive Rats

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