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      Difference in the effects of switching from Candesartan to Olmesartan or Telmisartan to Olmesartan in hypertensive patients with type 2 diabetes: the COTO study

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          This open-label controlled study compared the therapeutic efficacy of three representative angiotensin II receptor blockers (ARBs) in hypertensive patients with type 2 diabetes attending a hospital outpatient clinic. The primary measure in this study was morning home blood pressure (BP).

          Patients and methods

          Two studies were done concurrently to investigate the effects of switching from two different ARBs to olmesartan. Patients prescribed candesartan (8 mg once daily in the morning) or telmisartan (40 mg once daily in the morning) for 16 weeks were switched to olmesartan (20 mg once daily in the morning) for 16 weeks. Then, they were switched back to candesartan (CO group) or telmisartan (TO group) for another 16 weeks.


          Data from all patients in the CO group (n=165) and the TO group (n=152) were analyzed. Clinic and morning home BP and urinary albumin levels showed a significant decrease from baseline at 16 weeks after switching to olmesartan in both the CO and the TO group (clinic BP, morning home diastolic BP, and urinary albumin, P<0.05; morning home systolic BP, P<0.01). In contrast, clinic BP, morning home BP, and urinary albumin were significantly increased again 16 weeks after switching back to candesartan or telmisartan (clinic BP, morning home diastolic BP, and urinary albumin, P<0.05; morning home systolic BP, P<0.01). No subjects experienced an adverse reaction that required withdrawal from the study. No adverse reactions attributable to the study drugs were observed.


          Olmesartan is a promising ARB for BP control in hypertensive type 2 diabetics.

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          Most cited references 18

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          Identification of telmisartan as a unique angiotensin II receptor antagonist with selective PPARgamma-modulating activity.

          The metabolic syndrome is a common precursor of cardiovascular disease and type 2 diabetes that is characterized by the clustering of insulin resistance, dyslipidemia, and increased blood pressure. In humans, mutations in the peroxisome proliferator-activated receptor-gamma (PPARgamma) have been reported to cause the full-blown metabolic syndrome, and drugs that activate PPARgamma have proven to be effective agents for the prevention and treatment of insulin resistance and type 2 diabetes. Here we report that telmisartan, a structurally unique angiotensin II receptor antagonist used for the treatment of hypertension, can function as a partial agonist of PPARgamma; influence the expression of PPARgamma target genes involved in carbohydrate and lipid metabolism; and reduce glucose, insulin, and triglyceride levels in rats fed a high-fat, high-carbohydrate diet. None of the other commercially available angiotensin II receptor antagonists appeared to activate PPARgamma when tested at concentrations typically achieved in plasma with conventional oral dosing. In contrast to ordinary antihypertensive and antidiabetic agents, molecules that can simultaneously block the angiotensin II receptor and activate PPARgamma have the potential to treat both hemodynamic and biochemical features of the metabolic syndrome and could provide unique opportunities for the prevention and treatment of diabetes and cardiovascular disease in high-risk populations.
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            The Japanese Society of Hypertension Guidelines for the Management of Hypertension (JSH 2009).

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              Effect of dosing time of angiotensin II receptor blockade titrated by self-measured blood pressure recordings on cardiorenal protection in hypertensives: the Japan Morning Surge-Target Organ Protection (J-TOP) study.

              To study the impact of the dosing time of an angiotensin II receptor blocker (ARB) titrated by self-measured home blood pressure (HBP) on cardiorenal damage in hypertensives. We conducted an open-label multicenter trial, the J-TOP study, that enrolled 450 hypertensives with self-measured systolic HBP more than 135 mmHg. The study patients were stratified into three groups according to the difference between their morning and evening SBPs difference: a morning hypertension group (morning and evening difference at least 15 mmHg; n = 170), a morning and evening hypertension group (0 mmHg < or = morning and evening difference <15 mmHg; n = 198), and an evening hypertension group (morning and evening difference <0 mmHg; n = 82). Individuals were then randomly allocated to receive bedtime dosing or awakening dosing of candesartan (+/- diuretic as needed) titrated to achieve a target systolic HBP less than 135 mmHg. The 6-month change in the urinary albumin/creatinine ratio (UACR) was assessed. In total patients, the UACR was more markedly reduced in the bedtime-dosing group than in the awakening-dosing group (-45.7 vs. -34.5%, P = 0.02), whereas there were no differences in the reduction of any of the HBPs including the sleep blood pressures (BPs) between the two groups. Among the three subgroups stratified by the morning and evening difference, the difference in the UACR reduction between the bedtime-dosing and awakening-dosing groups was only significant in the morning hypertension group (-50.6 vs. -31.3%, P = 0.02). In HBP-guided antihypertensive treatment in hypertensives, bedtime dosing of an ARB may be superior to awakening dosing for reducing microalbuminuria.

                Author and article information

                Drug Des Devel Ther
                Drug Des Devel Ther
                Drug Design, Development and Therapy
                Dove Medical Press
                17 February 2014
                : 8
                : 219-226
                Department of Internal Medicine, Sakaide City Hospital, Kagawa, Japan
                Author notes
                Correspondence: Hiroyuki Daikuhara, Department of Internal Medicine, Sakaide City Hospital, 1-6-43 Bunkyocho, Sakaide, Kagawa 762-0031, Japan Tel +81 877 465 131, Fax +81 877 462 377, Email daikusan@ 123456r5.dion.ne.jp
                © 2014 Daikuhara et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License

                The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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