Cerivastatin prevents angiotensin II-induced renal injury independent of blood pressure- and cholesterol-lowering effects

Park, Joon-Keun; Müller, Dominik N.; Mervaala, Eero; Dechend, Ralf; Fiebeler, Anette; Schmidt, Folke; Bieringer, Markus; Schäfer, O.; Lindschau, Carsten; Schneider, Wolfgang; Ganten, Detlev; Luft, Friedrich C.; Haller, Hermann

doi:10.1046/j.1523-1755.2000.00304.x

Cited by 156 publications

(114 citation statements)

References 42 publications

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“…[1][2][3] Therefore, the ability of statins to inhibit ICAM-1 expression indicates that statins can attenuate leukocyte-endothelial cell interactions and the subsequent endothelial damage and tissue injury. Indeed, many studies have reported that statins can inhibit leukocyte-endothelial cell interactions in many conditions, such as thrombin-activated leukocyte-endothelial cell interactions, 47 angiotensin II-induced injury, 35,48 transient ischemic injury, 36,49 and Staphylococcus aureus ␣-toxin-induced inflammation. 14 These results provide the best evidence to support the view that statins can inhibit leukocyte-endothelial cell interactions independent of their lipid-lowering effect.…”

Section: Discussionmentioning

confidence: 99%

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Simvastatin Inhibits Leukocyte Accumulation and Vascular Permeability in the Retinas of Rats with Streptozotocin-Induced Diabetes

Miyahara

Kiryu

Yamashiro

et al. 2004

The American Journal of Pathology

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Section: Discussionmentioning

confidence: 99%

“…[33][34][35][36][47][48][49] These differences may derive from the diversity of the mechanisms of each model or duration of the drug administration. In addition, many studies with streptozotocin-induced diabetic animals were performed for a relatively short duration compared to chronic diabetes in human.…”

Section: Discussionmentioning

confidence: 99%

Simvastatin Inhibits Leukocyte Accumulation and Vascular Permeability in the Retinas of Rats with Streptozotocin-Induced Diabetes

Miyahara

Kiryu

Yamashiro

et al. 2004

The American Journal of Pathology

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“…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). A link between ANG II-induced generation of oxygen radicals and cellular hypertrophy was demonstrated in aortas of mice genetically deficient in gp91 phox (40) and in mouse renal tubular cells transfected with p22 phox antisense (16), two membrane-bound NADPH oxidase subunit proteins.…”

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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“…10,11 Rats were purchased from RCC Ltd (Fuellinsdorf, Switzerland). Experiments were conducted in 4-week-old male dTGR (nϭ28) and nontransgenic, age-matched Sprague-Dawley (SD; Tierzucht Schoenwalde, Germany; nϭ7) rats after due approval (permit No.…”

Section: Animal Groups and Physiological Measurementsmentioning

confidence: 99%

Aldosterone Potentiates Angiotensin II–Induced Signaling in Vascular Smooth Muscle Cells

et al. 2004

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Background-In a double-transgenic human renin and human angiotensinogen rat model, we found that mineralocorticoid receptor (MR) blockade ameliorated angiotensin II (Ang II)-induced renal and cardiac damage. How Ang II and aldosterone (Ald) might interact is ill defined. Methods and Results-We investigated the effects of Ang II (10 Ϫ7 mol/L) and Ald (10 Ϫ7 mol/L) on extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) signaling in vascular smooth muscle cells (VSMCs) with Western blotting and confocal microscopy. Ang II induced ERK 1/2 and JNK phosphorylation by 2 minutes. Ald achieved the same at 10 minutes. Ang IIϩAld had a potentiating effect by 2 minutes. Two oxygen radical scavengers and the epidermal growth factor receptor (EGFR) antagonist AG1478 reduced Ang II-, Ald-, and combination-induced ERK1/2 phosphorylation. Preincubating the cells with the MR blocker spironolactone (10 Ϫ6 mol/L) abolished Ang II-induced ROS generation, EGFR transactivation, and ERK1/2 phosphorylation. Conclusions-Ald potentiates Ang II-induced ERK-1/2 and JNK phosphorylation. Oxygen radicals, the MR, and the EGFR play a role in early signaling induced by Ang II and Ald in VSMCs. These in vitro data may help explain the effects of MR blockade on Ang II-induced end-organ damage in vivo.

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Cerivastatin prevents angiotensin II-induced renal injury independent of blood pressure- and cholesterol-lowering effects

Cited by 156 publications

References 42 publications

Simvastatin Inhibits Leukocyte Accumulation and Vascular Permeability in the Retinas of Rats with Streptozotocin-Induced Diabetes

Simvastatin Inhibits Leukocyte Accumulation and Vascular Permeability in the Retinas of Rats with Streptozotocin-Induced Diabetes

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

Aldosterone Potentiates Angiotensin II–Induced Signaling in Vascular Smooth Muscle Cells

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