Lowering of Elevated Ambulatory Blood Pressure by HMG-CoA Reductase Inhibitors

Terzoli, L.; Mircoli, Luca; Raco, Roberta; Ferrari, Alberto

doi:10.1097/01.fjc.0000175432.56789.e6

Cited by 37 publications

(31 citation statements)

References 13 publications

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“…56 In contrast, no effect was observed in normotensive subjects. 56 Hypertensive and dyslipidaemic subjects (n ¼ 32) were treated with atorvastatin (20 mg/day) in one study.…”

mentioning

confidence: 61%

“…These findings were independent of lipid-lowering associated with statin treatment. 55 In another study, 56 hypertensive and normotensive subjects with hypercholesterolaemia were randomised to receive a statin (n ¼ 51, simvastatin 10-20 mg/day, pravastatin 10-20 mg/day or atorvastatin 5-10 mg/day) or placebo (n ¼ 23) for 2 months. Statin-treated hypertensive subjects showed lower systolic and diastolic ambulatory BP (À5.775.8 and À3.573.9 mm Hg, respectively, both Po0.001).…”

Section: Do Lipid Abnormalities Predict the Risk For Hypertension?mentioning

confidence: 99%

“…56 In contrast, no effect was observed in normotensive subjects. 56 Hypertensive and dyslipidaemic subjects (n ¼ 32) were treated with atorvastatin (20 mg/day) in one study. 57 In the Brisighella Heart Study, 59 a total of 1356 HC subjects were randomly treated for 5 years with either low-fat diet, cholestyramine, gemfibrozil or simvastatin.…”

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confidence: 97%

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Statins: another class of antihypertensive agents?

et al. 2006

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The assessment of global cardiovascular risk is an essential step in the management of atherosclerotic disease prevention. Among the risk factors to be addressed are hypertension and hyperlipidaemia; these commonly coexist. A neutral or lipid-friendly antihypertensive agent is probably useful in the presence of lipid abnormalities. Similarly, statins have been shown to decrease cardiovascular risk in hypertensive patients. There is also experimental and clinical evidence that statins have blood pressure (BP)-lowering effects. In this review, we discuss the beneficial effects of statins on BP, and provide an overview of the underlying pathophysiology. We also consider the evidence justifying the use of statins in the management of hypertensive patients.

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“…56 In contrast, no effect was observed in normotensive subjects. 56 Hypertensive and dyslipidaemic subjects (n ¼ 32) were treated with atorvastatin (20 mg/day) in one study.…”

mentioning

confidence: 61%

Section: Do Lipid Abnormalities Predict the Risk For Hypertension?mentioning

confidence: 99%

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Statins: another class of antihypertensive agents?

et al. 2006

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“…Terzoli et al [32] performed a clinical study to address the conflicting results regarding blood pressurelowering effect of statins. Patients with cholesterol >200 mg/dL and no previous statin treatment underwent 24-h ABP monitoring and were classified as normotensives or hypertensives according to their ABP.…”

Section: In Patients Without Hypertensionmentioning

confidence: 99%

Are statins effective for simultaneously treating dyslipidemias and hypertension?

2008

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Abstract3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) are unequivocally useful for lowering cholesterol levels in patients with dyslipidemias characterized by elevations in total and/or low-density lipoprotein cholesterol. The beneficial effects of statins to lower serum cholesterol translate into significant reductions in cardiovascular morbidity and mortality. In addition to lowering cholesterol levels, statins have other biological effects relevant to cardiovascular homeostasis including anti-inflammatory actions and downregulation of angiotensin type 1 receptor expression that contribute to improvements in enodthelial function and arterial compliance. Since enodthelial dysfunction and reduced arterial compliance are important pathophysiological determinants of essential hypertension, these actions of statins raise the possibility that statin therapy may be useful for simultaneously treating dyslipidemias and hypertension. However, it has been unclear whether statins are effective in lowering blood pressure. This controversy stems from a variety of methodological limitations including inadequate sample size, confounding effects of antihypertensive drugs, differences in blood pressure measurement techniques, and differences in patient populations. However, based on published results from both small clinical studies and large randomized clinical trials, statins modestly lower blood pressure in patients with high, but not normal, blood pressure, regardless of cholesterol level.

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“…Several clinical trials have demonstrated that statins exert beneficial effects in patients at high cardiovascular risk. 10 Moreover, several studies have shown that statins decrease blood pressure in variable degrees both in humans [11][12][13][14] and in experimental models, 15,16 although a lack of effect of statins on blood pressure levels has also been described. [17][18][19] Most of the benefits of statin therapy are attributable to the lowering of serum cholesterol levels.…”

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confidence: 99%

Atorvastatin Prevents Angiotensin II–Induced Vascular Remodeling and Oxidative Stress

et al. 2009

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Abstract-Angiotensin II (Ang II) modulates vasomotor tone, cell growth, and extracellular matrix deposition. This study analyzed the effect of atorvastatin in the possible alterations induced by Ang II on structure and mechanics of mesenteric resistance arteries and the signaling mechanisms involved. Wistar rats were infused with Ang II (100 ng/kg per day, SC minipumps, 2 weeks) with or without atorvastatin (5 mg/kg per day). Ang II increased blood pressure and plasmatic malondialdehyde levels. Compared with controls, mesenteric resistance arteries from Ang II-treated rats showed the following: (1) decreased lumen diameter; (2) increased wall/lumen; (3) decreased number of adventitial, smooth muscle, and endothelial cells; (4) increased stiffness; (5) increased collagen deposition; and (6) diminished fenestrae area and number in the internal elastic lamina. Atorvastatin did not alter blood pressure but reversed all of the structural and mechanical alterations of mesenteric arteries, including collagen and elastin alterations. In mesenteric resistance arteries, Ang II increased vascular O 2 ⅐Ϫ production and diminished endothelial NO synthase and CuZn/superoxide dismutase but did not modify extracellular-superoxide dismutase expression. Atorvastatin improved plasmatic and vascular oxidative stress, normalized endothelial NO synthase and CuZn/superoxide dismutase expression, and increased extracellularsuperoxide dismutase expression, showing antioxidant properties. Atorvastatin also diminished extracellular signalregulated kinase 1/2 activation caused by Ang II in these vessels, indicating an interaction with Ang II-induced intracellular responses. In vascular smooth muscle cells, collagen type I release mediated by Ang II was reduced by different antioxidants and statins. Moreover, atorvastatin downregulated the Ang II-induced NADPH oxidase subunit, Nox1, expression. Our results suggest that statins might exert beneficial effects on hypertension-induced vascular remodeling by improving vascular structure, extracellular matrix alterations, and vascular stiffness. These effects might be mediated by their antioxidant properties.

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Lowering of Elevated Ambulatory Blood Pressure by HMG-CoA Reductase Inhibitors

Cited by 37 publications

References 13 publications

Statins: another class of antihypertensive agents?

Statins: another class of antihypertensive agents?

Are statins effective for simultaneously treating dyslipidemias and hypertension?

Atorvastatin Prevents Angiotensin II–Induced Vascular Remodeling and Oxidative Stress

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