In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth muscle contraction and blood vessel constriction. This vasoconstriction effect increases the resistance to blood flow in the peripheral parts of the body, leading to an increase in blood pressure.
The activation of the AT1 receptor also stimulates the secretion of aldosterone, a hormone that promotes sodium and water retention in the kidneys, increasing blood volume and pressure. Angiotensin receptor blockers (ARBs) such as losartan and valsartan are used to treat high blood pressure. These medications compete with angiotensin II to bind to the AT1 receptor and deactivate it, reducing vasoconstriction. As a result, blood vessels dilate, peripheral resistance decreases, and blood pressure is reduced. AT1 receptor blockage also suppresses aldosterone secretion, which decreases sodium and water reabsorption by the kidneys and lowers blood volume and pressure. Unlike ACE inhibitors, which increase bradykinin levels, leading to a dry cough, ARBs do not have this effect, resulting in no dry cough.
