PPARα Activator Effects on Ang II–Induced Vascular Oxidative Stress and Inflammation

Diep, Quy N.; Amiri, Farhad; Touyz, Rhian M.; Cohn, Jeffrey S.; Endemann, Dierk; Neves, Mário Fritsch; Schiffrin, Ernesto L.

doi:10.1161/01.hyp.0000037969.41360.cc

Cited by 220 publications

(179 citation statements)

References 44 publications

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“…6 K Studies confirmed that oxidative stress has a central role in altered endothelial function by changes in nitric oxide (NO) biosynthesis. 25 What this study adds K No studies regarding the associations of reactive oxygen species (ROS) with blood pressure and arterial stiffness have been done in black South Africans. K Oxidative stress contributes to increased blood pressure in African men, especially hypertensive men.…”

Section: Discussionmentioning

confidence: 99%

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Associations between reactive oxygen species, blood pressure and arterial stiffness in black South Africans: the SABPA study

et al. 2011

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Many mechanisms, including oxidative stress, contribute to hypertension. This study investigated the possible associations between oxidative stress, blood pressure and arterial stiffness in black South Africans. Ambulatory blood pressure measurements were taken for 101 black South African men and 99 women. The stiffness indices included ambulatory arterial stiffness index (AASI) and pulse pressure (PP). Reactive oxygen species (ROS) levels (Po0.0001) were higher in the African women compared with men. ROS levels were also higher in hypertensive compared with normotensive men. The 24 h systolic blood pressure (SBP; Po0.01), 24 h diastolic blood pressure (DBP; Po0.0001) and pulse wave velocity (PWV; Po0.01) were significantly higher in African men compared with women. There were unadjusted positive associations of 24 h SBP (r ¼ 0.33; P ¼ 0.001), 24 h DBP (r ¼ 0.26; P ¼ 0.008) and 24 h PP (r ¼ 0.29; P ¼ 0.003) with ROS in African men only. A positive association between AASI and ROS existed only in hypertensive men (r ¼ 0.27; P ¼ 0.035), but became nonsignificant (B ¼ 0.0014; P ¼ 0.14) after adjustments. Adjusted, positive associations of 24 h SBP (B ¼ 0.181; P ¼ 0.018) and 24 h PP (B ¼ 0.086; P ¼ 0.050) with ROS were again only evident in African men. ROS is positively associated with SBP and PP in African men, suggesting that increased ROS levels may contribute to hypertension in this population group.

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Section: Discussionmentioning

confidence: 99%

“…25 It is clear that one could not pinpoint a specific factor contributing to the onset and/or maintenance of hypertension, but rather explore the vast collection of contributing factors. It is evident from this study that ROS seems to have a role in cardiovascular dysfunction, as reflected by the association with SBP and PP in the men.…”

Section: Discussionmentioning

confidence: 99%

Associations between reactive oxygen species, blood pressure and arterial stiffness in black South Africans: the SABPA study

et al. 2011

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“…Under pathological conditions, increased ROS bioactivity leads to endothelial dysfunction, increased contractility, vascular smooth muscle cells growth, monocyte invasion, lipid peroxidation, inflammation, and increased deposition of extracellular matrix proteins, important factors in hypertensive vascular damage. 27,28 Despite the preponderance of evidence for the association of increased oxidative stress with various vascular diseases, using antioxidants to prevent CVD has produced mixed outcomes. 29,30 This article highlights current developments in the field of ROS and hypertension, focusing specifically on the role of oxidative stress in hypertensionassociated vascular damage.…”

Section: Discussionmentioning

confidence: 99%

Total antioxidant status and oxidative DNA damage in a South Indian population of essential hypertensives

et al. 2010

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To investigate the total antioxidant status (TAS) and the extent of oxidative DNA damage in total lymphocytes and their relation with essential hypertension. A total of 130 South Indian subjects aged 30-65 were recruited for the study. Of these hypertensive subjects investigated, 30 were newly diagnosed and were not on any antihypertensive drugs, but had systolic blood pressure (BP) ranging between 140 and 160 mm Hg and diastolic BP between 95 and 100 mm Hg; 50 hypertensive patients who were already on drug therapy for 1 year and 50 were normotensive controls with BP p120/80 mm Hg. DNA damage was significantly increased in hypertensive patients (both newly diagnosed and who were already on drug therapy) compared with control group. The major increase in DNA damage was observed in newly diagnosed hypertensive patients compared with hypertensive patients who were already on drug therapy. There was a significant decrease in plasma TAS value in essential hypertensive groups as compared to normotensive controls. Lymphocyte DNA damage was independently correlated with only TAS. Lymphocyte DNA damage was increased in hypertensive patients. The major increase in lymphocyte DNA damage was observed in newly diagnosed hypertensive patients compared with hypertensive patients who already on drug therapy. Decreased TAS levels, which reflect to increased oxidative stress, may be the reason of increased total lymphocyte DNA damage in South Indian hypertensive patients.

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“…22,23 The fixative was washed from the organ bath by repeated changes with PBS (pH 7.4) and finally washed with PBS containing 0.1% Triton X-100 (pH 8.0). Arteries were incubated with 0.5% BSA/PBS for 5 minutes at 42°C.…”

Section: Laser Confocal Microscopymentioning

confidence: 99%

Angiotensin Type 2 Receptor in Resistance Arteries of Type 2 Diabetic Hypertensive Patients

et al. 2007

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Abstract-The role of angiotensin type 2 receptor (AT 2 R) on vascular responses to angiotensin II in humans remains unclear. In this study we explored whether AT 2 R is expressed and functionally active on peripheral resistance arteries of hypertensive diabetic patients treated for 1 year with either the angiotensin receptor blocker valsartan or the ␤-blocker atenolol. Twenty-six hypertensive type 2 diabetic patients treated with oral hypoglycemic and antihypertensive agents (not receiving angiotensin receptor blockers or ␤-blockers) were randomly assigned to double-blind treatment for 1 year with valsartan or atenolol once daily added to their previous therapy in a clinical trial that we reported recently and compared with 10 normal subjects. Resistance arteries dissected from gluteal subcutaneous tissues were assessed on a pressurized myograph. Vasomotor response curves to angiotensin II (1 nmol/L to 1 mol/L) were performed on norepinephrine precontracted vessels in the presence of valsartan (10 mol/L) with or without the AT 2 R inhibitor PD123319 (1 mol/L). AT 2 R expression was evaluated by confocal microscopy. After 1 year of treatment, systolic and diastolic blood pressure was controlled and comparable in the valsartan and atenolol groups. Angiotensin II evoked a significant vasodilatory response only on resistance arteries from patients treated with valsartan, effect blocked by PD123319. AT 2 R expression was 4-fold higher in small arteries of valsartan-treated patients. A ngiotensin II (Ang II) is the main biological effector of the renin-angiotensin system, which plays a major role in cardiovascular and renal homeostasis. Most of the physiological and pathophysiological effects of Ang II are mediated by the angiotensin type 1 receptor (AT 1 R), which is widely expressed by most cell types. Expression of the angiotensin type 2 receptor (AT 2 R) is more limited and occurs predominantly in fetal tissues where it may play a role during development. 1,2 Recent studies, mostly in cellular and adult animal models, mapped the distribution of AT 2 R in certain areas of the brain, 3 kidneys, 4 coronary arteries, cardiomyocytes, ventricular myocardium, 5 and the vasculature. 6,7 Increased AT 2 R expression has been observed under pathological conditions, such as vascular injury, 8 hypertension, 6,7 myocardial infarction, 9,10 congestive heart failure, 11 renal failure, 12 and brain ischemia. 13 Few studies have investigated the functional expression of AT 2 R in humans. AT 2 Rs are expressed in the human skin (throughout the epidermal and dermal structures) 14 and are markedly upregulated in incisional cutaneous wounds. 15 AT 2 Rs have been demonstrated in the human coronary microcirculation, where they may contribute to vasodilation. 16 Studies in cellular and animal models suggest that AT 2 R counteracts many AT 1 R actions by inducing vasodilation, antiproliferation, and apoptosis. 2 We showed recently in animal models of hypertension that AT 2 R is upregulated and mediates vasodilation only when AT 1 Rs are bl...

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PPARα Activator Effects on Ang II–Induced Vascular Oxidative Stress and Inflammation

Cited by 220 publications

References 44 publications

Associations between reactive oxygen species, blood pressure and arterial stiffness in black South Africans: the SABPA study

Associations between reactive oxygen species, blood pressure and arterial stiffness in black South Africans: the SABPA study

Total antioxidant status and oxidative DNA damage in a South Indian population of essential hypertensives

Angiotensin Type 2 Receptor in Resistance Arteries of Type 2 Diabetic Hypertensive Patients

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