At1 receptor

The AT1 receptor is a G-protein-coupled receptor, which is present in two isoforms. The activated receptor binds to the proteins Gq/11 and Gi/o, which activates phospholipase C and increases the concentration of calcium Ca2+ in the cytosol. This then mediates effects such as vasoconstriction and stimulation of protein kinase C at the molecular level. In addition to the vascular system and heart, the AT1 receptor can also be expressed in the brain, kidney and adrenal glands as well as in the liver and intestine.

Activating the AT1 receptor causes the following effects:

• increase in blood pressure (increase in vascular resistance due to vasoconstriction, increase in cardiac contractility)
• Promotion of the release of noradrenaline from the sympathetic nerve endings
• Promotion of renal water and saline retention
• Promotes the synthesis and release of aldosterone. Note: the renin-angiotensin system (RAA) is therefore also called renin-angiotensin-aldosterone system (RAAS).
• Inhibition of the release of renin. Paradoxically, this is due to an IP3-iduced increase in the cytosolic Ca concentration in JG cells which leads to an inhibition of the cellular cAMP concentration. Since an increase in cytosolic Ca concentration normally leads u to a stimulation of the cell, but has the opposite effect here, this phenomenon is called the calcium paradox of renin release.

AT1 receptors mediate cardiovascular remodeling after myocardial infarction (remodeling)

AT1 receptor blockers are drugs that bind with high affinity to the AT1 receptor and thus suppress the effect of angiotensin II mediated by these receptors.