Antioxidants Block Angiotensin II-Induced Increases in Blood Pressure and Endothelin

Ortiz, Mariela; Manriquez, Melissa C.; Romero, J. Carlos; Juncos, Luis A.

doi:10.1161/01.hyp.38.3.655

Cited by 125 publications

(140 citation statements)

References 28 publications

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“…Several studies have shown that acute administration of tempol can inhibit or reduce the hemodynamic actions of acute or chronic Ang II (Nishiyama el al., 2001;Zhang et al, 2004;Lopez et al, 2003). Using long-term tempol treatment, Ortiz et al found that tempol at 1 mM in the drinking water blocked Ang II induced hypertension and oxidative stress (Ortiz et al, 2001). However, the ability of tempol to lower arterial pressure in their studies may be related to the very low dose of Ang II (5 ng/kg/min) compared to the current study (approximately 200 ng/kg/min).…”

Section: Discussioncontrasting

confidence: 55%

“…The increase in ROS production may play a role in the elevation of blood pressure by a direct vasoconstrictor effect or indirectly by reducing the activity of vasodilators such as NO and arachidonic acid metabolites (Reckelhoff and Romero, 2003). Studies have also shown that treatment with liposome-encapsulated superoxide dismutase (SOD) or the membrane-permeable SOD mimetic, tempol, markedly blunts the increase in blood pressure caused by chronic, low-dose Ang II administration, suggesting that stimulation of ROS formation is critically involved in the blood pressure response to Ang II (Laursen et al, 1997;Nishiyama et al, 2001;Ortiz et al, 2001;Kawada et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

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Synergistic actions of enalapril and tempol during chronic angiotensin II-induced hypertension

Elmarakby

Imig

Pollock

et al. 2007

Vascular Pharmacology

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Experiments were designed to test the hypothesis that antioxidant treatment would increase the antihypertensive actions of endogenous kinins during angiotensin converting enzyme (ACE) inhibition. Four groups of rats, all given angiotensin II (Ang II) for 2 weeks, were studied: 1) control, 2) enalapril, 3) tempol or 4) both tempol and enalapril. Ang II significantly increased systolic blood pressure (BP) when compared with the baseline (170± 8 vs. 128± 4 mm Hg, P<0.05). Neither enalapril nor tempol alone was able to attenuate the elevation in BP (165± 7 and 164± 6 mm Hg, respectively). In contrast, combined administration of tempol and enalapril prevented the increase in BP (137± 5 mmHg). Plasma 8-isoprostane increased in Ang II infused rats when compared with control untreated rats (69± 14 vs. 23± 0.5 pg/ml, P<0.05). Tempol alone or tempol plus enalapril significantly attenuated the increase in plasma 8-isoprostane (29± 6 and 34± 7 pg/ml, respectively). In additional experiments, we used the bradykinin B 2 antagonist, icatibant to determine if increased B 2 receptor contributes to the antihypertensive effect of combined tempol and enalapril in Ang II infused rats. Icatibant decreased the ability of this combination to lower arterial pressure. Additionally, a significant increase in B 1 receptor protein expression in renal cortex of Ang II infused rats was observed compared to control suggesting that the bradykinin receptors activation could account for the effect of enalapril to enhance the actions of tempol. These data support the hypothesis that combined reduction of superoxide along with enhanced endogenous kinins may facilitate blood pressure lowering in Ang II hypertension.

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Section: Discussioncontrasting

confidence: 55%

Section: Introductionmentioning

confidence: 99%

Synergistic actions of enalapril and tempol during chronic angiotensin II-induced hypertension

Elmarakby

Imig

Pollock

et al. 2007

Vascular Pharmacology

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“…8-iso PGF 2␣ can be generated by a non-enzymatic oxidative reaction of arachidonic acid (28,29). Measurements of 8-iso PGF 2␣ have been used to quantitate oxidative stress in vitro and in vivo (15,17,39). We demonstrated that the renal excretion of 8-iso PGF 2␣ was increased in the mice infused with AngII400.…”

Section: Discussionmentioning

confidence: 90%

A Mouse Model of Angiotensin II Slow Pressor Response

Kawada

Imai

Karber³

et al. 2002

Journal of the American Society of Nephrology

179

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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“…A growing body of evidence points to the free radicals production as one of the major factors involved in cardiovascular and renal alterations associated with ANG II hypertension. Treatment with superoxide dismutase (SOD) reduced spontaneous tone of aorta isolated from rats infused with ANG II (39) and SOD (19) or SOD mimetic (29,30) blunted hypertension induced by ANG II in rats. Inhibition of the HMGCoA reductase with various statins was reported to reduce arterial pressure and to prevent cardiac hypertrophy and renal injury in models of ANG II-dependent hypertension (31,45).…”

Section: Discussionmentioning

confidence: 99%

Sodium restriction prevents cardiac hypertrophy and oxidative stress in angiotensin II hypertension

Rugale¹,

Delbosc

Cristol

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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Rugale, Caroline, Sandrine Delbosc, Jean-Paul Cristol, Albert Mimran, and Bernard Jover. Sodium restriction prevents cardiac hypertrophy and oxidative stress in angiotensin II hypertension. Am J Physiol Heart Circ Physiol 284: H1744-H1750, 2003. First published December 5, 2002 10.1152/ajpheart.00864.2002The influence of a low-sodium (LS) diet was assessed on the cardiac and renal alterations and pro-oxidant effect associated with a 10-day infusion of angiotensin II (200 or 400 ng ⅐ kg Ϫ1 ⅐ min Ϫ1 , osmotic pumps). Tail-cuff pressure (TCP), albuminuria, and renal blood flow were determined at the end of the experiments. Heart weight index (HWI) and production of superoxide anion (O 2 Ϫ ⅐) by the left ventricle and H2O2 by the aorta was measured with the use of bioluminescence. Although the final TCP was similar in LS and normal sodium (NS) rats infused with high and low doses of angiotensin II, respectively, the increase in HWI was prevented by the LS diet. Sodium restriction reduced the rise in albuminuria without a change in the renal effect of angiotensin II. The increased production of O 2 Ϫ ⅐ and H2O2 observed in NS rats was abrogated in LS rats. The beneficial influence of dietary sodium restriction on target organ damage induced by angiotensin II is independent of arterial pressure reduction and possibly related to attenuation of the prooxidant effect of the peptide. heart weight; albuminuria; reactive oxygen species; renal hemodynamic THE DEVELOPMENT OF cardiac hypertrophy results from the interaction between several factors, including elevated arterial pressure, angiotensin II (ANG II), and sodium intake. Although blood pressure is an important determinant of cardiac mass (8), ANG II may directly increase protein synthesis and cause myocyte hypertrophy, as reported in cultured cardiac myocytes isolated from chicks (2) and neonatal rats (34). In vivo long-term administration of an initially subpressor dose of ANG II, a model that mimics the development of human hypertension, induces a gradual rise in blood pressure associated with a cardiac hypertrophy (7,14,17). However, ANG II might increase cardiac mass independently of arterial pressure. This was suggested by the presence of cardiac hypertrophy in rats infused with a nonpressor dose of the peptide (4, 37) or in rats infused with a pressor dose of ANG II and concomitantly treated by hydralazine (7, 37).The concentration of sodium ion in vitro or dietary sodium intake in vivo may modulate cardiac mass. In cultured neonatal rat myocardial myoblasts, cellular protein content and cell size increased when sodium concentration of the medium was augmented (15). In vivo, a high-sodium intake increased cardiac mass in normotensive rats (46) and exacerbated cardiac hypertrophy in hypertensive rats (12). In humans, sodium intake (assessed by urinary sodium excretion) and the left ventricular mass index were positively correlated in hypertensive and normotensive subjects (9). Conversely, a low-sodium (LS) intake prevents cardiac hypertrophy associated with two-k...

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Antioxidants Block Angiotensin II-Induced Increases in Blood Pressure and Endothelin

Cited by 125 publications

References 28 publications

Synergistic actions of enalapril and tempol during chronic angiotensin II-induced hypertension

Synergistic actions of enalapril and tempol during chronic angiotensin II-induced hypertension

A Mouse Model of Angiotensin II Slow Pressor Response

Sodium restriction prevents cardiac hypertrophy and oxidative stress in angiotensin II hypertension

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