Correlativity between blood measures related to blood stasis blocking collaterals and gene expression of angiotensin-converting enzyme of renal cortex in diabetic rats and effect of stasis removing and collaterals dredging

Summary: Background: Angiotensin-converting-enzyme inhibitors (ACEI) and angiotensin II receptor blockers (ARB) are widely used as a first-line therapy for the treatment of cardiovascular disease. Here, ACEI modulate the bradykinin receptor (BDKRB1 and BDKRB2) system and NO-dependent endothelial function, thus determining cardiovascular health and regenerative arteriogenesis. The current study aims at evaluating nitric oxide-dependent endothelial function, and gene expression of bradykinin receptors in peripheral blood mononuclear cells (PBMC) from patients with ACEI or ARB treatment. Patients and methods: The WalkByLab has been established to screen cardiovascular patients for peripheral artery disease and coronary artery disease. In total 177 patients from WalkByLab with heterogenous disease and risk status were randomly selected, divided according to their medication history into the following groups: 1. ACEI group, 2. ARB group or 3. non-ACE/ARB group. Total plasma nitrite/nitrate (NO) levels were measured, endothelial function was evaluated by assessing flow meditated dilation (FMD). PBMC were isolated from peripheral whole blood, and gene expression (qRT-PCR) of bradykinin receptors and angiotensin converting enzyme were assessed. Results: Plasma total NO concentration in the ACEI group (24.66±16.28, µmol/l) was increased as compared to the ARB group (18.57±11.58, µmol/l, P=0.0046) and non-ACE/ARB group (16.83±8.64, µmol/l, P=0.0127) in patients between 40 to 90 years of age. However, FMD values (%) in the ACEI group (7.07±2.40, %) were similar as compared to the ARB (6.35±2.13, %) and non-ACE/ARB group (6.51±2.15, %), but significantly negatively correlated with age. Interestingly, BDKRB1 mRNA level was significantly higher and BDKRB2 mRNA level lower in the ACEI group (BDKRB1 3.88-fold±1.05, BDKRB2 0.22-fold±0.04) as compared to the non-ACE/ARB group (BDKRB1 1.00-fold±0.39, P<0.0001, BDKRB2 1.00-fold±0.45, P=0.0136). Conclusions: ACEI treatment enhances total nitrite/nitrate concentration, furthermore, upregulates BDKRB1 in PBMC, but downregulates BDKRB2 mRNA expression. FMD is a strong determinant of vascular aging and is sensitive to underlying heterogenous cardiovascular diseases.

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Effect of Combination of Angiotensin-Converting Enzyme Inhibitors and Vitamin D Receptor Activators on Cardiac Oxidative Stress in Diabetic Rats

The American Journal of the Medical Sciences ◽

10.1016/j.amjms.2016.04.016 ◽

2016 ◽

Vol 352 (2) ◽

pp. 208-214 ◽

Cited By ~ 3

Author(s):

Tarek Mohamed Ali ◽

Osama Mahmoud Mehanna ◽

Amgad Gaber Elsaid ◽

Ahmad El Askary

Keyword(s):

Oxidative Stress ◽

Vitamin D ◽

Angiotensin Converting Enzyme ◽

Vitamin D Receptor ◽

Enzyme Inhibitors ◽

Angiotensin Converting Enzyme Inhibitors ◽

Diabetic Rats ◽

Converting Enzyme ◽

Converting Enzyme Inhibitors

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Lemon Extract Reduces Angiotensin Converting Enzyme (ACE) Expression and Activity and Increases Insulin Sensitivity and Lipolysis in Mouse Adipocytes

Nutrients ◽

10.3390/nu12082348 ◽

2020 ◽

Vol 12 (8) ◽

pp. 2348

Author(s):

Shilpa Tejpal ◽

Alan M. Wemyss ◽

Claire C. Bastie ◽

Judith Klein-Seetharaman

Keyword(s):

Gene Expression ◽

Insulin Sensitivity ◽

Angiotensin Converting Enzyme ◽

Protein Expression ◽

Serum Insulin ◽

Fold Increase ◽

Cardiovascular Complications ◽

Lemon Juice ◽

Converting Enzyme ◽

Ace Gene

Obesity is associated with insulin resistance and cardiovascular complications. In this paper, we examine the possible beneficial role of lemon juice in dieting. Lemon extract (LE) has been proposed to improve serum insulin levels and decrease angiotensin converting enzyme (ACE) activity in mouse models. ACE is also a biomarker for sustained weight loss and ACE inhibitors improve insulin sensitivity in humans. Here, we show that LE impacts adipose tissue metabolism directly. In 3T3-L1 differentiated adipocyte cells, LE improved insulin sensitivity as evidenced by a 3.74 ± 0.54-fold increase in both pAKT and GLUT4 levels. LE also induced lipolysis as demonstrated by a 16.6 ± 1.2 fold-change in pHSL protein expression levels. ACE gene expression increased 12.0 ± 0.1 fold during differentiation of 3T3-L1 cells in the absence of LE, and treatment with LE decreased ACE gene expression by 80.1 ± 0.5% and protein expression by 55 ± 0.37%. We conclude that LE’s reduction of ACE expression causes increased insulin sensitivity and breakdown of lipids in adipocytes.

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