Cardioprotection

Renin-angiotensin-aldosterone inhibitors have shown to promote cardioprotection by reducing superoxide production and the level of stress in the endoplasmic reticulum in coronary artery cells. These effects are important to maintain vascular integrity.

 

Angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs) or mineralocorticoid receptor blockers may inhibit the activation of the renin-angiotensin-aldosterone system (RAAS, a hormone system involved in the regulation of blood sodium concentrations and arterial blood pressure). They can provide cardioprotection by reducing the activation of RAAS with consequent impact on the concentration of substances such as superoxide (SO) and on the amount of stress in the endoplasmic reticulum (ER). Both SO production and ER stress determine vascular integrity.

An article published in the International Journal of Cardiology by researchers from the University of Florida, College of Medicine analyzed ER stress and SO generation in human coronary artery endothelial cells (HCAEC) in the presence of RAAS blockers. HCAEC were cultured with blood pressure-lowering drugs spironolactone, captopril, lisinopril, candesartan and losartan, and recombinant human insulin. ER stress was measured by placental alkaline phosphatase (ES-TRAP) assay. The superoxide generation was determined by chemiluminescence. ER stress and SO production were inhibited by knocking down or blocking the AT1 receptor and spironolactone. ACE inhibitors were only effective in reducing oxidative stress. Insulin added into the culture media did not alter SO production or ER stress.

It was possible to identify that the AT1 receptor mediates ER stress and oxidative stress (through SO production). RAAS inhibitors may have cardioprotective properties, suggesting that they could be an important pharmacological strategy against cardiovascular diseases and diabetes-related vascular complications.

 

 

 

Written By: Vagner Raso

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