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Query: UMLS:C0011849 (diabetes)
277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the treatment for the hypertension patients with diabetes mellitus, the target blood pressure is below 130/80mmHg. As the first choice drugs, ARB, ACE inhibitor and Ca channel blocker are recommended. In the high normal blood pressure patient (130-139/80-89mmHg), the initial approach is life-style modification. In hypertension patients with diabetes (over 140/90mmHg), blood pressure should be controlled with the medication. The life-style modification should be performed even in the patients treated with anti-hypertensive drugs.
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PMID:[Treatment for hypertension with diabetes mellitus]. 1708 2

Type 2 diabetes has long been known to be associated with an increased risk of cardiovascular disease. Patients with type 2 diabetes have also been shown to benefit more from antihypertensive therapy than do non-diabetics with hypertension. The benefits of aggressive antihypertensive therapy are reflected in the recent reduction of blood pressure (BP) targets in international guidelines. Drugs acting on the renin-angiotensin-aldosterone system (RAAS) have well-documented efficacy, and results from large-scale trials with highly selective angiotensin II (Ang II) receptor blockers (ARBs), such as valsartan, are awaited. The VALUE trial will provide the largest body of information yet on the comparative benefits of using an ARB or calcium channel blocker in hypertensive patients with diabetes.
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PMID:Cardiac, renal and vascular complications in the diabetic patient. 1719 15

Angiotensin-converting enzyme (ACE) inhibitors have a well-established role in the management of patients with hypertension, diabetes, heart failure and myocardial infarction (MI). ACE inhibitors have been particularly well studied in acute and chronic MI with consistent and substantial survival benefits demonstrated, particularly in the higher risk groups. The recent development of angiotensin II (Ang II) receptor blockers (ARBs) as a well tolerated pharmacological therapy to more completely inhibit the actions of Ang II at the AT1-receptor level raises questions concerning comparative efficacy with the proven ACE inhibitor experience. Two major trials will provide a direct comparison of ARBs with an ACE inhibitor. The Valsartan in Acute Myocardial Infarction (VALIANT) trial is specifically designed to compare and contrast the ARB, valsartan, used both alone as well as in combination with a proven ACE inhibitor regimen, in a high risk MI population. VALIANT, with its three arms targetting 14,500 patients, is uniquely poised to determine whether the pharmacological advance in the development of ARBs confers additional clinical (survival) value in high risk MI patients.
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PMID:Will more complete inhibition of the RAAS with angiotensin receptor blockade improve survival following myocardial infarction? 1719 21

The metabolic syndrome is a syndrome characterized by visceral obesity, and is associated with lipid abnormalities, hypertension, and hyperglycemia. The prevalence of this syndrome is increasing in Japan, mainly because of widespread lifestyle changes. Studies from our and other laboratories have shown that early intervention with an ARB can attenuate the development of hypertension in animal models, with a similar trend found in the recent TROPHY clinical study. ARBs also cause inhibition of new-onset diabetes, and may have beneficial effects on insulin resistance and lipid metabolism. The results of multiple laboratory studies and clinical trials suggest that early intervention with ARBs will play an increasing role in preventing progression of the metabolic syndrome and its complications.
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PMID:[Use of angiotensin receptor blockers (ARBs) in the metabolic syndrome]. 1730 87

This editorial considers the use of the first selective oral renin inhibitor, aliskiren, in reducing angiotensin (Ang) II reactivation or aldosterone (ALDO) escape during renin-angiotensin-aldosterone system (RAAS) inhibition. RAAS blockade with angiotensin converting enzyme inhibitors (ACEIs) and/or angiotensin receptor AT(1) blockers (ARBs) is very useful for the treatment of arterial hypertension, chronic heart failure (CHF), atherosclerosis and diabetes. 'Ang II reactivation' and 'ALDO escape' or 'breakthrough' have been observed during either ACEI or ARB treatment, and may attenuate the clinical benefit of RAAS blockade. Renin and Ang I accumulate during ACE inhibition, and might overcome the ability of an ACEI to effectively suppress ACE activity. There is also data suggesting that 30 - 40% of Ang II formation in the healthy human during RAAS activation is formed via renin-dependent, but ACE-independent, pathways. Moreover, ACE gene polymorphisms contribute to the modulation and adequacy of the neurohormonal response to long-term ACE inhibition, at least in patients with CHF (up to 45% of CHF patients have elevated Ang II levels despite the long-term use of an ACEI) or diabetes. The reactivated Ang II promotes ALDO secretion and sodium reabsorption. ALDO breakthrough also occurs during long-term ARB therapy, mainly by an AT(2)-dependent mechanism. This was related to target-organ damage in animal models. Oral renin inhibition with aliskiren has showed excellent efficacy and safety in the treatment of hypertension. Aliskiren can be co-administered with ACEIs, ARBs or hydrochlorothiazide. Furthermore, there is evidence suggesting that aliskiren reduces Ang II reactivation in ACE inhibition and ALDO escape during treatment with an ACEI or an ARB, at least to the degree that this is associated with the RAAS. For RAAS-independent ALDO production, the combination of aliskiren with eplerenone might prove useful.
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PMID:Angiotensin II reactivation and aldosterone escape phenomena in renin-angiotensin-aldosterone system blockade: is oral renin inhibition the solution? 1737 10

This project assesses the treatment role with insulin and (or) angiotensin II receptor subtype-1 (AT1-R) blocker (ARB) on insulin receptor and endothelin-1 receptor subtype (ETA-R and ETB-R) regulation in rat hearts suffering from insulin-dependent diabetes mellitus (IDDM). Animals were divided into 6 groups: groups 1, 3, and 5 were controls consisting of normal, diabetic (streptozotocin-treated, once at 0 time), and diabetic supplemented daily with insulin, respectively, whereas groups 2, 4, and 6 were the controls treated daily with losartan. One month after enrollment, rats were sacrificed and samples of cardiac tissue were snapped frozen for immunostaining and Western blotting. Insulin receptor density was observed to be upregulated in the cardiomyocytes of diabetic animals, but downregulated with insulin supplementation alone. Cotreatment with insulin and an ARB resulted in drastic increase in insulin-receptor density in the diabetic rats. In addition, expression of ETA-R in cardiomyocytes was upregulated and was consistently maintained within the various treatment modalities. However, ETB-R expression was significantly reduced in the diabetic group treated with both insulin and an ARB. The changes in the expression of the insulin, the ETA-Rs, and the ETB-Rs at the various sites of the myocardium and the effect of both insulin treatment and blockade of the AT1-R explain the new benefits related to the halting of myocardial remodeling in IDDM rats.
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PMID:Effect of type-1 diabetes mellitus on the regulation of insulin and endothelin-1 receptors in rat hearts. 1748 63

More than 1 medication is required in many hypertensive patients to reach blood pressure (BP) goals, and initial treatment with 2 agents has been recommended for patients whose BP level is >20/10 mm Hg above target. Diuretics reduce BP levels and the incidence of target organ complications and together with angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers, which are recommended in patients with comorbid cardiovascular disease, nephropathy, or diabetes, are effective antihypertensive combinations. Calcium channel blockers (CCBs) are also effective antihypertensive agents, and evidence suggests that a CCB/ACEI combination is well tolerated and also decreases the risk of cardiovascular and renal disease. Some evidence suggests that this combination may improve endothelial function more than either agent alone, and its use could potentially lead to better cardiovascular outcomes than a diuretic/ACEI or diuretic/ARB combination. The ongoing Avoiding Cardiovascular Events Through Combination Therapy in Patients Living With Systolic Hypertension (ACCOMPLISH) trial compares these 2 effective combinations (ie, an ACEI/diuretic and ACEI/CCB) as initial treatment for reducing cardiovascular morbidity and mortality in older high-risk hypertensive patients. The results of this trial, when reported, should help to clarify the relative benefits of these different therapies.
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PMID:Combination therapy with an angiotensin-converting enzyme inhibitor and a calcium channel blocker. 1791 6

Diabetic nephropathy is a major cause of end-stage renal failure (ESRF) in patients with both type 1 and type 2 diabetes. Many factors such as genetic and non-genetic promoters, hypertension, hyperglycemia, accumulation of advanced glycation end products (AGEs), dyslipidemia, albuminuria and proteinuria influence the progression of this disease. It is important to determine pathogenesis and treatment of this disease. However, it is difficult to investigate since human diabetes is a heterogeneous and multifactorial disease. Therefore, most of these mechanisms have been investigated in animal experiments. KK/Ta mice have a clearly different genetic background in terms of body weight, blood glucose, impaired glucose tolerance (IGT), urinary albumin excretion and serum triglyceride than BALB/c mice. Renal lesions of KK/Ta mice closely resemble those in human early diabetic nephropathy. Thus, the KK/Ta mouse may serve as a suitable model for the study of type 2 diabetes and early diabetic nephropathy in humans. We reviewed genetic susceptibility using genome-wide linkage analysis and differential display polymerase chain reaction (DD-PCR) or Northern blot analysis, and treatment of diabetic nephropathy using angiotensin type 1 (AT1) receptor blockers (ARB) or thiazolidinediones (TZDs) in KK/Ta mice.
Curr Diabetes Rev 2005 Aug
PMID:Pathogenesis and treatment of type 2 diabetic nephropathy: lessons from the spontaneous KK/Ta mouse model. 1822 Jun 4

New onset diabetes (NOD) is common among hypertensive patients, whether they are being treated for hypertension or not, and is associated with subsequently increased cardiovascular disease (CVD). Thiazide-like diuretics and beta-blockers are more likely to provoke hyperglycemia when compared with drugs that block the renin-angiotensin system, and calcium channel blockers. However, in contrast to the NOD arising during treatment with other antihypertensive drugs, the NOD that occurs during diuretic treatment, has not been shown to increase CVD, either in clinical trials, or during longer observational studies. In fact, blood pressure reduction achieved by diuretic treatment may avert the expected increase of CVD in NOD. Conventional blood pressure reduction (along with lipid lowering) is the proven approach to preventing CVD in diabetes, in whatever circumstances the diabetes occurs. Apprehensions relating to the potential onset of NOD should not influence the choice of the initial antihypertensive treatment choice, nor should it invariably lead to discontinuation of diuretics (although such a step may reverse hyperglycemia). NOD can also sometimes be eliminated by correcting hypokalemia with a potassium-sparing diuretic, and/or potassium supplementation, or by adding a potassium-conserving antihypertensive drug such as an ACEI, ARB, or an anti-aldosterone agent. If all these stratagems fail (or are unsuitable), and the diuretic is essential to blood pressure control, then hypoglycemic therapy is indicated. NOD does adversely affect quality of life, and is not to be accepted lightly. However, diuretic-induced hyperglycemia can be managed, and should be tolerated if a diuretic is essential for blood pressure control. In summary, the potential for occurrence of NOD certainly needs consideration, but it is not an insurmountable challenge, and must not compromise aggressive blood pressure control, which remains the primary tool for antihypertensive care.
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PMID:New onset diabetes during antihypertensive therapy. 1843 39

Several factors have been incriminated in the genesis of diabetic nephropathy. To elucidate their interplay, we have used a hypertensive, obese, diabetic rat model with nephropathy (SHR/NDmcr-cp) that mimics human type 2 diabetes. This model is characterized by hypertension, obesity with the metabolic syndrome, diabetes with insulin resistance, and intrarenal advanced glycation end product (AGE) accumulation. In order to achieve renoprotection, which was evaluated by histology and albuminuria, various therapeutic approaches were used: caloric restriction, antihypertensive agents (angiotensin II receptor blocker [ARB] and calcium channel blocker), lipid- (bezafibrate) or glucose-lowering (insulin and pioglitazone) agents, and cobalt chloride (a hypoxia-inducible factor activator). Altogether, renoprotection is not necessarily associated with blood pressure or glycemic control. By contrast, it is almost always associated with decreased AGE formation, with the exception of insulin, which induces hyperinsulinemia, eventually leading to an overproduction of transforming growth factor-beta. AGE formation is reduced directly by in vitro active compounds (e.g., ARBs) or indirectly by in vitro inactive compounds (e.g., pioglitazone and cobalt). In the latter cases, AGE reduction may reflect a decreased oxidative stress as it is concomitant with a marked reduction of oxidative stress markers. It remains to be seen whether the renoprotection offered by these various approaches may be additive.
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PMID:Inhibition of advanced glycation end products: an implicit goal in clinical medicine for the treatment of diabetic nephropathy? 1844 8


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