AT2 receptor: Its role in obesity associated hypertension.

The renin-angiotensin system (RAS) is a hormonal cascade that acts together to regulate blood pressure. Angiotensin II (Ang II) is the major octapeptide of RAS and mediates its cellular and physiological actions by acting on AT₁ and AT₂ receptor. Most of the cellular and physiological actions of Ang II such as cellular growth and proliferation, vasoconstriction, antinatriuresis and increase in blood pressure are mediated via AT₁ receptor. The functions associated with the AT₂ receptors are less studied, in part, due to its lower expression in adult tissues. However, AT₂ receptor has been suggested as functional antagonist of AT₁ receptors and thereby opposes the actions of Ang II mediated via AT₁ receptor. Thus, the activation of AT₂ receptors has been shown to cause vasodilatation, natriuresis and decrease in blood pressure. After the discovery of the AT₂ receptor in various parts of the kidney, including in proximal tubules, there has been an interest in establishing a link between the renal AT₂ receptor, renal Na-excretion and blood pressure regulation. Earlier, we have reported that activation of renal AT₂ receptors increases urinary Na excretion in obese Zucker rats, in part via inhibiting Na⁺/K⁺- ATPase (NKA) activity and stimulating nitric oxide/cGMP pathway in the proximal tubules. An impaired pressure natriuresis and increased AT₁ receptor function is believed to be the cause of hypertension in obese Zucker rats and other animal models of obesity. In this review, we are focussing on the role of renin angiotensin system especially AT₂ receptors in obesity associated hypertension.