Role of Angiotensin and Oxidative Stress in Essential Hypertension

Romero, J. Carlos; Reckelhoff, Jane F.

doi:10.1161/01.hyp.34.4.943

Cited by 313 publications

(238 citation statements)

References 74 publications

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“…We demonstrated that the renal excretion of 8-iso PGF 2␣ was increased in the mice infused with AngII400. This extends to the mouse the original observation of Romero et al in rat and swine that prolonged slow pressor infusion of AngII increased the plasma level of 8-iso PGF 2␣ (3). Tempol is a membrane permeant nitroxide that acts as an SOD mimetic.…”

Section: Discussionsupporting

confidence: 58%

See 1 more Smart Citation

A Mouse Model of Angiotensin II Slow Pressor Response

Kawada

Imai

Karber³

et al. 2002

Journal of the American Society of Nephrology

182

183

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Abstract. The slow pressor response to prolonged infusions of angiotensin II (AngII) entails a delayed rise in BP. This study investigated the hypothesis that the response depends on the generation of oxidative stress. The BP and renal functional response of mice to graded doses (200, 400, and 1000 ng · kg Ϫ1 · min Ϫ1 ) of subcutaneously infused AngII was studied. The SBP of conscious mice increased by day 3 at AngII1000 but showed a delayed rise by days 9 to 13 (slow pressor response) at the lower rates of AngII infusion. By day 13, there was a graded increase in SBP with the rate of AngII infusion (Vehicle, Ϫ2.6 Ϯ 2.6%; AngII200, ϩ14.1 Ϯ 5.0%; AngII400, ϩ31.9 Ϯ 1.9%; AngII1000, ϩ43.2 Ϯ 5.5%). The MAP measured under anesthesia rose significantly (P Ͻ 0.001) with AngII400 at 14 d (Vehicle, 85 Ϯ 2 mmHg; AngII400, 100 Ϯ 3 mmHg). When studied at day 6, the MAP of AngII400 rats was not elevated (88 Ϯ 2 mmHg; NS versus vehicle), yet the GFR was higher (1.05 Ϯ 0.05 versus 1.25 Ϯ 0.05 ml · min Ϫ1 · g Ϫ1 ; P Ͻ 0.05) accompanied by an increase in the filtration fraction (FF) (28.8 Ϯ 1.2 versus 37.2 Ϯ 0.8%; P Ͻ 0.001). From day 6 through day 14, the MAP had increased (P Ͻ 0.01) in AngII400, accompanied by a significant reduction in GFR to 1.05 Ϯ 0.04 ml · min Ϫ1 · g Ϫ1 (P Ͻ 0.01) and elevation of renal vascular resistance (RVR) (day 6 versus day 14, 15.3 Ϯ 0.6 versus 19.2 Ϯ 1.2 mmHg · ml Ϫ1 · min Ϫ1 · g Ϫ1 ; P Ͻ 0.05). Renal excretion of 8-iso PGF 2␣ was increased in AngII400 group at day 12 (2.52 Ϯ 0.35 versus 5.85 Ϯ 0.78 pg · day Ϫ1 ; P Ͻ 0.01). The permeant superoxide dismutase mimetic tempol reduced the effects of AngII400 on the SBP (Ϫ1.7 Ϯ 5.8%; P Ͻ 0.01), the MAP (87 Ϯ 4 mmHg; P Ͻ 0.01), and the RVR (15.2 Ϯ 0.5 mmHg · ml Ϫ1 · min Ϫ1 · g Ϫ1 ; P Ͻ 0.05) at day 14 and the renal 8-iso PGF 2␣ excretion (3.53 Ϯ 0.71 pg · d Ϫ1 ; P Ͻ 0.05) at day 12. It is concluded that the AngII infused mouse is a valid model for the slow pressor response. There is an early rise in GFR and FF, consistent with increased postglomerular vascular resistance and a late rise in RVR with a fall in GFR, consistent with increased preglomerular vascular resistance that is accompanied by a rise in BP. There is evidence of increased oxidative stress that is implicated in the increase in the BP and RVR in this model.The angiotensin II (AngII) slow pressor response is a gradually developing increase in BP (BP) with an initially subpressor rate of infusion (1-4). The slow pressor response was first described in rats in 1963, (1) and subsequently has been demonstrated in rabbits, dogs and man (5). Whereas the plasma AngII levels increase by about 80-fold during an immediate pressor response, they are elevated within a physiologic level of 2-to sixfold during a slow pressor response (6). A slow pressor response is seen also with the thromboxane A2/prostaglandin H2 (TP) receptor mimetic, U-46619 (7,8). This slow pressor response has been considered an excellent model for renal hypertension in which both AngII type I (AT1) and TP receptor have been implica...

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Section: Discussionsupporting

confidence: 58%

“…The angiotensin II (AngII) slow pressor response is a gradually developing increase in BP (BP) with an initially subpressor rate of infusion (1)(2)(3)(4). The slow pressor response was first described in rats in 1963, (1) and subsequently has been demonstrated in rabbits, dogs and man (5).…”

mentioning

confidence: 99%

A Mouse Model of Angiotensin II Slow Pressor Response

Kawada

Imai

Karber³

et al. 2002

Journal of the American Society of Nephrology

182

183

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“…9 It has been shown that DNA damage contributes significantly to the development and progression of atherosclerosis. 10 Although increased levels of reactive oxygen species (ROS) 11,12 and decreased antioxidant capacity were investigated, the relationship between lymphocyte DNA damage and total antioxidant status (TAS) has not been investigated in both newly diagnosed and during therapy of essential hypertensive patients, so far.…”

Section: Introductionmentioning

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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“…1 Excessive production of reactive oxygen species (ROS), which outstrip antioxidant defence mechanisms, has been implicated in pathophysiological conditions that impact on the CV system. Hypertension is considered a state of oxidative stress (OX) that can contribute to the development of artherosclerosis 2 and other hypertension-induced organ damage. 3 Assessment of antioxidant activities and lipid peroxidation byproducts in hypertensives indicates an excessive amount of ROS and a reduction of antioxidant mechanism activity in blood, as well as in several other cellular systems, 4 including not only vascular wall cells, 5 but also those cells found in circulating blood.…”

Section: Introductionmentioning

confidence: 99%

Impact of the components of metabolic syndrome on oxidative stress and enzymatic antioxidant activity in essential hypertension

et al. 2006

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The objective of the present study was to analyze the impact of metabolic syndrome (MS) and its individual components on oxidative stress (OX) and on the activity of antioxidant enzymes of patients with essential hypertension. One hundred and eighty-seven hypertensives, 127 (61.9%) of them having criteria for MS according to the International Diabetes Federation criteria and 30 healthy normotensive subjects were included. OX status was assessed by measuring glutathione oxidized/glutathione reduced and reactive oxygen species-induced byproducts of lipid peroxidation, malondialdehide, and DNA damage, 8-oxo-dG genomic and mitochondrial. Antioxidant enzymatic activity of Cu/Zn extracellular-superoxide dismutase (SOD) and catalase (CAT) was measured in plasma and glutathione peroxidase 1 in hemolysad erythrocytes. In mononuclear cells, total-SOD activity, CAT and glutathione peroxidase 1, were assessed as well. The OX state in both blood and peripheral mononuclear cells observed in hypertensives were not enhanced by the addition of components of the so-called MS. Likewise, the reduction in the activity of antioxidant enzymes, both extracellular and cytoplasmic, was not affected by the presence of additional components of the MS. Neither the number of components nor the individual addition of each of them, low high-density lipoprotein, triglycerides, abdominal obesity or fasting glucose, further impact in the OX abnormalities observed in those with only hypertension in absence of other components. In conclusion, the present data indicates that contribution of MS components to the OX burden generated by high blood pressure is minimal.

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Role of Angiotensin and Oxidative Stress in Essential Hypertension

Cited by 313 publications

References 74 publications

A Mouse Model of Angiotensin II Slow Pressor Response

A Mouse Model of Angiotensin II Slow Pressor Response

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

Impact of the components of metabolic syndrome on oxidative stress and enzymatic antioxidant activity in essential hypertension

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