Effects of angiotensin II receptor antagonist on endothelial vasomotor function and urinary albumin excretion in type 2 diabetic patients with microalbuminuria

Tan, Kathryn Choon Beng; Chow, Wing-Sun; Ai, Victor; Lam, Karen Siu Ling

doi:10.1002/dmrr.255

Cited by 44 publications

(28 citation statements)

References 37 publications

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“…type 2 diabetes; p22 phox ; endothelium-dependent relaxation; NADPH SUBSTANTIAL CLINICAL AND EXPERIMENTAL evidence suggest that vascular diseases are currently the principal causes of morbidity and mortality in patients with type 1 and type 2 diabetes mellitus (6). In patients with type 2 diabetes, insulin resistance as well as endothelial dysfunction appears to precede the development of hyperglycemia (38,44,45). Therefore, endothelial dysfunction may be a critical early target for preventing cardiovascular disease.…”

mentioning

confidence: 99%

Enhanced p22^phoxexpression impairs vascular function through p38 and ERK1/2 MAP kinase-dependent mechanisms in type 2 diabetic mice

Kassan

Choi

Galán

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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Type 2 diabetes is associated with vascular complication. We hypothesized that increased nicotinamide adenine dinucleotide phosphate (NADPH) oxidase subunit p22 phox expression impairs vascular endothelium-dependent relaxation (EDR) in type 2 diabetes. Type 2 diabetic (db Ϫ /db Ϫ ) and control (db Ϫ /db ϩ ) mice were treated with reactive oxygen species (ROS) scavenger, polyethylene glycol superoxide dismutase (1,000 U/kg daily ip), or small interfering RNA p22 phox (p22 phox -lentivirus-small interfering RNA, 100 g iv, 2 times/ wk) for 1 mo. EDR was impaired in microvascular bed (coronary arteriole and femoral and mesenteric resistance arteries) from diabetic mice compared with control. Interestingly, ROS scavenger and p22 phox downregulation did not affect blood glucose level or body weight but significantly improved EDR. Mitogen-activated protein kinases (ERK1/2 and p38) phosphorylation and NADPH oxidase activity were increased in arteries from diabetic mice and were reduced after ROS scavenger or p22 phox downregulation in db Ϫ /db Ϫ

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mentioning

confidence: 99%

Enhanced p22^phoxexpression impairs vascular function through p38 and ERK1/2 MAP kinase-dependent mechanisms in type 2 diabetic mice

Kassan

Choi

Galán

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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“…84 A number of studies have specifically assessed the ARB valsartan. [85][86][87][88][89][90] The details and findings of these studies are summarized in Table A3 below. Overall, the studies are consistent with the renoprotective effect of ARBs, however, they do not provide additional data allowing a direct comparison with ACEi.…”

Section: Studies Not Covered By Systematic Reviewsmentioning

confidence: 99%

Prevention and management of chronic kidney disease in type 2 diabetes

Chadban¹,

Howell²,

Twigg³

et al. 2010

Nephrology

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GUIDELINESBlood glucose control should be optimized aiming for a general HbA1c target 27%. (Grade A*). In people with type 2 diabetes and microalbuminuria or macroalbuminuria, angiotensin receptor blocker (ARB) or angiotensin-converting enzyme inhibitor ACEi antihypertensives should be used to protect against progression of kidney disease. (Grade A*). The blood pressure (BP) of people with type 2 diabetes should be maintained within the target range. ARB or ACEi should be considered as antihypertensive agents of first choice. Multi-drug therapy should be implemented as required to achieve target blood pressure. (Grade A*) People with type 2 diabetes should be informed that smoking increases the risk of chronic kidney disease (CKD) (Grade B*). Table A1: Definition of NHMRC grades of recommendation. Also refer to NHMRC 'National Evidence Based Guidelines for Diagnosis, Prevention and Management of CKD in Type 2 Diabetes' (see http://www.cari.org.au) for Levels of Evidence and Evidence Grading which were undertaken in accordance with the NHMRC Hierarchy of Evidence procedure. *Refer to SUGGESTIONS FOR CLINICAL CARE• The HbA1c target may need to be individualized taking in to account history of hypoglycaemia and co-morbidities. (refer to NHMRC Evidence Based Guideline for Blood Glucose Control in Type 2 Diabetes at http://www.nhmrc.gov.au).• Systolic blood pressure (SBP) appears to be the best indicator of the risk of CKD in type 2 diabetes. However, an optimum and safest lower limit of SBP has not been clearly defined.• In people with type 2 diabetes antihypertensive therapy with ARB or ACEi decreases the rate of progression of albuminuria, promotes regression to normoalbuminuria, and may reduce the risk of decline in renal function.• Due to potential renoprotective effects, the use of ACEi or ARB should be considered for the small subgroup of people with normal BP who have type 2 diabetes and microalbuminuria.• The extent to which interventions with lipid lowering therapy reduces the development of CKD in people with type 2 diabetes is unclear. As there is limited evidence relating to effects of lipid treatment on the progression of CKD in people with type 2 diabetes, blood lipid profiles should be managed in accordance with guidelines for prevention and management of cardiovascular disease (CVD).• Lifestyle modification (diet and physical activity) is an integral component of diabetes care (refer to the NHMRC Evidence Based Guidelines for Blood Glucose Control in Type 2 Diabetes), however, there are insufficient studies of suitable quality to enable dietary recommendations to be made with respect to prevention and/or management of CKD in people with type 2 diabetes. BACKGROUND Aim of the guidelineThis guideline topic has been taken from the NHMRC 'National Evidence Based Guidelines for Diagnosis, Prevention and Management of CKD in Type 2 Diabetes' which can be found in full at the CARI website (http:// www.cari.org.au). The NHMRC guideline covers issues related to the assessment and prevention of CKD in individu...

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“…Endothelial dysfunction has received increasing attention as a potential contributor to the pathogenesis of vascular disease in diabetes mellitus. Under physiological conditions, there is a balanced release of endothelial-derived relaxing and contracting factors, but this delicate balance is altered in diabetes and atherosclerosis, thereby contributing to further progression of vascular and end-organ damage (Tan et al, 2002). Hyperglycemia is the major causal factor in the development of endothelial dysfunction in diabetes mellitus.…”

Section: Introductionmentioning

confidence: 99%

Endothelial Dysfunction and Therapeutic Intervention in Type 2 Diabetes

Páez¹

2011

Medical Complications of Type 2 Diabetes

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Effects of angiotensin II receptor antagonist on endothelial vasomotor function and urinary albumin excretion in type 2 diabetic patients with microalbuminuria

Abstract: Type 2 diabetic patients with microalbuminuria have impaired endothelium-dependent and -independent vasodilation. Treatment with low-dose losartan is sufficient to reduce microalbuminuria in these patients without alteration in endothelial function and systemic blood pressure.

Cited by 44 publications

References 37 publications

Enhanced p22^phoxexpression impairs vascular function through p38 and ERK1/2 MAP kinase-dependent mechanisms in type 2 diabetic mice

Enhanced p22^phoxexpression impairs vascular function through p38 and ERK1/2 MAP kinase-dependent mechanisms in type 2 diabetic mice

Prevention and management of chronic kidney disease in type 2 diabetes

Endothelial Dysfunction and Therapeutic Intervention in Type 2 Diabetes

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Effects of angiotensin II receptor antagonist on endothelial vasomotor function and urinary albumin excretion in type 2 diabetic patients with microalbuminuria

Abstract: Type 2 diabetic patients with microalbuminuria have impaired endothelium-dependent and -independent vasodilation. Treatment with low-dose losartan is sufficient to reduce microalbuminuria in these patients without alteration in endothelial function and systemic blood pressure.

Cited by 44 publications

References 37 publications

Enhanced p22phoxexpression impairs vascular function through p38 and ERK1/2 MAP kinase-dependent mechanisms in type 2 diabetic mice

Enhanced p22phoxexpression impairs vascular function through p38 and ERK1/2 MAP kinase-dependent mechanisms in type 2 diabetic mice

Prevention and management of chronic kidney disease in type 2 diabetes

Endothelial Dysfunction and Therapeutic Intervention in Type 2 Diabetes

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Enhanced p22^phoxexpression impairs vascular function through p38 and ERK1/2 MAP kinase-dependent mechanisms in type 2 diabetic mice

Enhanced p22^phoxexpression impairs vascular function through p38 and ERK1/2 MAP kinase-dependent mechanisms in type 2 diabetic mice