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Hypertension: A Companion to Brenner and Rector's The Kidney since the first edition, diet and nutrition, pharmacological treatment.
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The renin—angiotensin—aldosterone system RAAS , the main regulator of sodium and fluid balance in normal subjects and one of the major contributors to the pathogenesis of hypertension, also plays an important role in the pathogenesis of endothelial dysfunction Figure 5. Preclinical studies have demonstrated that activation of the Ang II type 1 AT1 receptor contributes to the development of atherosclerosis by mediating endothelial dysfunction.

These findings support the functional significance of Ang II in the generation of oxidative stress and atherosclerosis in this model. RAAS blockers improve endothelial function and have favorable vascular, metabolic, cardiac, and renoprotective effects. Olmesartan medoxomil is an inactive prodrug that is rapidly and completely bioactivated by ester hydrolysis in the gut wall to the pharmacologically active compound olmesartan. Its peak plasma concentrations are achieved between 1 and 3 hours with an elimination half-life of 12—18 hours.

Accumulation is not noted on long-term dosing. Olmesartan has minimal or no inhibitory activity on human cytochrome P Olmesartan reduces BP rapidly and effectively in hypertensive patients. Olmesartan reduces BP more effectively than other ARBs when administered at traditionally recommended starting doses.

A significantly greater reduction in sitting cuff diastolic BP at trough was demonstrated with olmesartan The reduction in mean hour diastolic BP with olmesartan 8. The reduction in mean hour systolic BP with olmesartan All drugs were well tolerated. Reductions in mean hour systolic and diastolic blood pressure with 4 different ARBs. The differences in BP reduction achieved with olmesartan compared with losartan and valsartan are attenuated when doses of the other ARBs are increased.

In a week, randomized, double-blind, forced-titration study, hypertensive patients were assigned to receive olmesartan 20 mg, losartan 50 mg, valsartan 80 mg, or placebo, all once daily. At week 8, doses were titrated to 50 mg twice daily for losartan and mg once daily for valsartan. Olmesartan remained at 40 mg once daily. Compared with placebo, all 3 medications significantly reduced mean seated diastolic BP from baseline.

There was no significant difference compared with valsartan. Olmesartan did not reduce mean seated systolic BP significantly compared with valsartan. Microalbuminuria is an early sign of glomerular endothelial dysfunction and is associated with progressive glomerulosclerosis, renal function loss, and development of overt pro-teinuria. Microalbuminuria is also associated with increased CV morbidity and mortality in both diabetic and nondiabetic subjects.

Participants had type 2 diabetes, normal kidney function, and at least one additional CV risk factor, including hypertension, but without microalbuminuria. Primary end point was time to onset of microalbuminuria, and secondary end points included renal and CV events.

Overall, CV morbidity and mortality were similar 3. The increased risk of CV mortality with olmesartan relative to placebo was attributed by the authors to possible hypotensive episodes in subjects with preexisting CV disease. Olmesartan has vasoprotective and anti-inflammatory effects that are unrelated to BP reduction.

Michael Clarkson

Hydrochlorothiazide Treatment with pravastatin alone did not significantly alter inflammation markers. This study demonstrated that olmesartan significantly reduces biochemical markers of inflammation by as early as 6 weeks of treatment, resulting in possible additional CV benefits independent of BP reduction.


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Olmesartan has a remedial effect on the remodeling of resistance vessels that result from hypertension-related target organ damage. Subcutaneous gluteal resistance arteries were examined on a pressurized myograph to evaluate vascular structure at baseline and after 1 year of treatment.


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  • Further, AIx, a marker of vascular stiffness and endothelial function discussed previously, fell significantly with olmesartan, but remained unchanged with atenolol. Central aortic pressure decreased significantly in both groups without differences between groups. Endothelial function has been shown to improve with olmesartan treatment independent of BP reduction. A prospective study assessed endothelium-dependent coronary dilation in 26 untreated hypertensive patients. Patients initially received olmesartan 20 mg or amlodipine 5 mg daily.

    Mean dose was olmesartan Serum SOD activity tended to increase with olmesartan, but not with amlodipine. The authors concluded that olmesartan, but not amlodipine, improved endothelium-dependent coronary function, and that these beneficial effects of olmesartan on coronary vasomotion might be mediated via an antioxidant property of the ARB. Olmesartan has been shown to reduce the volume of atherosclerotic plaque in patients with hypertension independent of BP reduction.

    The reductions in large plaques occurred despite similar reductions in BP, suggesting an antiatherosclerotic action of olmesartan that is independent of its BP lowering effect. Patients were randomly assigned to control without treatment with ACEIs or ARBs or olmesartan 10—40 mg titrated to maximally tolerated dose by 8 weeks.

    Follow-up IVUS showed significantly decreased progression in total atheroma volume 0. There were no significant differences in systolic and diastolic BP between groups either at baseline or month follow-up. Adherence rate is inversely related to the number of drugs given and occurrence of adverse effects. Compliance to the treatment is probably to increase if an antihypertensive agent combines these characteristics and, in addition, if patients are informed about extra protections of the medication.

    BP reduction is the most effective way to reduce CV risk in patients with hypertension. Some antihypertensive agents have additional benefits that are independent of BP. Dr Pimenta reports no conflicts of interest in this work. National Center for Biotechnology Information , U. Integr Blood Press Control. Published online Sep Eduardo Pimenta 1 and Suzanne Oparil 2. Author information Article notes Copyright and License information Disclaimer.

    Received Sep This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited. Keywords: hypertension, endothelial function, cardiovascular outcomes, olmesartan. Introduction The vascular endothelium is a thin layer of cells that line the interior surface of blood vessels separating circulating blood from layers of vascular smooth muscle cells VSMC. Open in a separate window. Figure 1.

    Agents that act continuously in the tone regulation of the vasculature.


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    • Endothelial function Nitric oxide and oxidative stress NO, originally described as EDRF, 1 is a free radical, short-lived, highly permeable gas. Clinical assessment of endothelial function Several techniques are available for the assessment of endothelial function in humans Table 1 , but all of these have limited applicability in clinical practice. Table 1 Methods for measuring endothelial function. Figure 2. Figure 3. Endothelial dysfunction: from hypertension to CV disease Endothelial dysfunction links hypertension with other CV risk factors that promote the development of atherosclerotic plaque, CV disease, and fatal and nonfatal CV events Figure 4.

      Figure 4. Figure 5. Mechanisms of action of angiotensin receptor blockers ARBs. Olmesartan Pharmacology Olmesartan medoxomil is an inactive prodrug that is rapidly and completely bioactivated by ester hydrolysis in the gut wall to the pharmacologically active compound olmesartan.

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      Protective effects of olmesartan Blood pressure Olmesartan reduces BP rapidly and effectively in hypertensive patients. Figure 6. Microalbuminuria Microalbuminuria is an early sign of glomerular endothelial dysfunction and is associated with progressive glomerulosclerosis, renal function loss, and development of overt pro-teinuria.

      Inflammation, vascular remodeling, and endothelial function Olmesartan has vasoprotective and anti-inflammatory effects that are unrelated to BP reduction. CV outcomes Olmesartan has been shown to reduce the volume of atherosclerotic plaque in patients with hypertension independent of BP reduction. Patient perspectives Adherence rate is inversely related to the number of drugs given and occurrence of adverse effects.

      Hypertension: A Companion to Brenner and Rector's The Kidney

      Conclusion BP reduction is the most effective way to reduce CV risk in patients with hypertension. Footnotes Disclosure Dr Pimenta reports no conflicts of interest in this work. References 1. The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine. Endothelial function and dysfunction: testing and clinical relevance. Pathophysiology, diagnosis and prognostic implications of endothelial dysfunction.

      Ann Med. Prognostic value of coronary vascular endothelial dysfunction. Spieker LE, luscher TF. Endothelium in hypertension:nitric oxide.

      UCC Research Profiles: Michael Clarkson, Medicine

      In: Oparil S, Weber M, editors. Philadelphia, PA: Elsevier Saunders; Vascular endothelial cells synthesize nitric oxide from L-arginine. L-arginine is the physiological precursor for the formation of nitric oxide in endothelium-dependent relaxation. Biochem Biophys Res Commun. Nitric oxide in hypertension. J Clin Hypertens Greenwich ; 8 12 Suppl 4 — Endothelial function and dysfunction.

      Part II: Association with cardiovascular risk factors and diseases. J Hypertens. Basal nitric oxide synthesis in essential hypertension. Hydroxy-methylglutaryl-coenzyme A reductase inhibition promotes endothelial nitric oxide synthase activation through a decrease in caveolin abundance. Part I: Methodological issues for assessment in the different vascular beds: a statement by the Working Group on Endothelin and Endothelial Factors of the European Society of Hypertension.

      Non-invasive detection of endothelial dysfunction in children and adults at risk of atherosclerosis. Expert consensus document on arterial stiffness: methodological issues and clinical applications. Eur Heart J. Etiology and pathogenesis of systemic hypertension. Philadelphia, PA: Elsevier; Exacerbation of atherosclerosis by hypertension. Potential mechanisms and clinical implications.

      Arch Intern Med. Benner and Rector's the Kidney, 7th edition 2 vol set. Complement and Kidney Disease. Kidney and Hypertension. The Aging Kidney in Health and Disease. The Kidney at a Glance. Kidney Cancer: Principles and Practice.

      ISBN 13: 9780721602585

      Obesity And the Kidney Contributions to Nephrology. Kidney and Blood Pressure Regulation. Veroeffentlichungen im Brenner Diseases of the Kidney and Urinary Tract. Genetic Diseases of the Kidney. Der Brenner und der liebe Gott. The Diabetic Kidney Contemporary Diabetes. Primer on Kidney Diseases. Kidney Research.