ADRB1 and triple-A syndrome: Although previous studies found a vital role of renin angiotensin aldosterone system (RAAS) activation in the pathogenesis of AAA and a close relation between β1AR and RAAS,[41, 42] β1AR is highly expressed in the heart but weakly expressed in VSMCs, as demonstrated by previous studies.[43] In the present study, high‐dose formoterol treatment resulted in a higher systolic pressure and heart rate in mice, suggesting a stimulating effect of formoterol on β1AR in the mouse heart, However, these effects may not be used to explain the adverse effect of high‐dose formoterol on AAA.