Alpha2A-adrenoceptors protect against hypertensive kidney disease.

What is it about?

The sympathetic nervous system is an important regulator in the cardiovascular and renal system of the human body. Increased sympathetic nerve activity plays an important role in hypertension and kidney disease. The α2A-adrenergic receptors (α2A-adrenoceptors), located prejunctional at the neuroeffector junction of sympathetically innervated organs act as autoreceptors by binding endogenous NE to inhibit its own release. This paper investigates the role of α2A-adrenergic receptors (α2A-adrenoceptors) in hypertension and hypertensive kidney disease.

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Why is it important?

Our finding shows that during experimental hypertension induced by angiotensin II, deletion of α2A-adrenoceptors increased renal NE release and activated specific sodium transporters within the kidney which are critical in hypertension. Knockout mice had significantly higher systolic BP and heightened kidney damage compared with wild-type mice. Reduction of sympathetic nerve activity by renal denervation attenuated hypertension and improved renal function in knockout mice. These findings show that α2A-adrenoceptors are important regulators of renal sympathetic outflow in hypertension and protect from hypertensive kidney disease.

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