Purpose of review: The renin-angiotensin system is a coordinated hormonal cascade important to the regulation of the renal sodium excretion and blood pressure. The major effector peptide, angiotensin II, binds two major receptors, AT1 and AT2. While the majority of angiotensin II actions are mediated via the AT1 receptor, evidence has accumulated that the AT2 receptor opposes the AT1 receptor, especially by inducing vasodilation instead of vasoconstriction.
Recent findings: During the past year, the evidence for an AT2 receptor microvascular dilator action has been presented that is mediated by nitric oxide (NO) generation in a bradykinin-dependent or independent manner. Although the AT2 receptor is expressed in renal proximal and distal tubules and vasculature, and AT2 receptor stimulation induces a bradykinin/NO pathway within the kidney, little information is available concerning AT2 receptor regulation of renal function and sodium excretion. From studies reported this year, the AT2 receptor appears to be protective against ischemic renal injury.
Summary: The AT2 receptor represents a potentially important area of investigation with therapeutic applications in the future.