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There is ample evidence supporting a role for angiotensin II type 2 receptor (AT 2 R) in counterbalancing the effects of angiotensin II (ang II) through the angiotensin II type 1 receptor by promoting vasodilation and having anti-inflammatory effects. Elastin insufficiency in both humans and mice results in large artery stiffness and systolic hypertension. Unexpectedly, mesenteric arteries from elastin insufficient ( Eln  +/− ) mice were shown to have significant vasoconstriction to AT 2 R agonism  in vitro  suggesting that AT 2 R may have vasoconstrictor effects in elastin insufficiency. Given the potential promise for the use of AT 2 R agonists clinically, the goal of this study was to determine whether AT 2 R has vasoconstrictive effects in elastin insufficiency  in vivo . To avoid off-target effects of agonists and antagonists, mice lacking AT 2 R ( Agtr2  −/ Y  ) were bred to  Eln  +/−  mice and cardiovascular parameters were assessed in wild-type (WT),  Agtr2  −/ Y  ,  Eln  +/− , and  Agtr2  −/ Y   ;Eln  +/−  littermates. As previously published,  Agtr2  −/ Y   mice were normotensive at baseline and had no large artery stiffness, while  Eln  +/−  mice exhibited systolic hypertension and large artery stiffness. Loss of AT 2 R in  Eln  +/−  mice did not affect large artery stiffness or arterial structure but resulted in significant reduction of both systolic and diastolic blood pressure. These data support a potential vasocontractile role for AT 2 R in elastin insufficiency. Careful consideration and investigation are necessary to determine the patient population that might benefit from the use of AT 2 R agonists.

Loss of Angiotensin II Type 2 Receptor Improves Blood Pressure in Elastin Insufficiency