Central Artery Hemodynamics in Angiotensin II-Induced Hypertension and Efects of Anesthesia

Systemic hypertension is a strong risk factor for cardiovascular, neurovascular, and renovascular diseases. Central artery stifness is both an initiator and indicator of hypertension, thus revealing a critical relationship between the wall mechanics and hemodynamics. Mice have emerged as a critical animal model for studying efects of hypertension and much has been learned. Regardless of the specifc mouse model, data on changes in cardiac function and hemodynamics are necessarily measured under anesthesia. Here, we present a new experimental-computational workfow to estimate awake cardiovascular conditions from anesthetized data, which was then used to quantify efects of chronic angiotensin II-induced hypertension relative to normotension in wild-type mice. We found that isofurane anesthesia had a greater impact on depressing hemodynamics in angiotensin II-infused mice than in controls, which led to unexpected results when comparing anesthetized results between the two groups of mice. Through comparison of the awake simulations, however, in vivo relevant efects of angiotensin II-infusion on global and regional vascular structure, properties, and hemodynamics were found to be qualitatively consistent with expectations. Specifcally, we found an increased in vivo vascular stifness in the descending thoracic aorta and suprarenal abdominal aorta, leading to increases in pulse pressure in the distal aorta. These insights allow characterization of the impact of regionally varying vascular remodeling on hemodynamics and mouse-to-mouse variations due to induced hypertension.