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

S E Hopper1, D Weiss2, N Mikush3

  • 1Department of Biomedical Engineering, University of Michigan, Ann Arbor, MI, USA.

PubMed

Insights

This study developed a method to estimate awake cardiovascular conditions in mice from anesthetized data. This revealed hypertension-induced vascular stiffness and altered hemodynamics, crucial for understanding cardiovascular disease.

Area of Science:

  • Cardiovascular Physiology
  • Biomedical Engineering
  • Animal Models in Hypertension Research

Background:

  • Systemic hypertension is a major risk factor for cardiovascular, neurovascular, and renovascular diseases.
  • Central artery stiffness is a key factor in hypertension, linking vascular mechanics and hemodynamics.
  • Mice are vital models for hypertension research, but hemodynamic data is typically collected under anesthesia.

Purpose of the Study:

  • To develop and validate an experimental-computational workflow to estimate awake cardiovascular conditions from anesthetized data in mice.
  • To quantify the effects of chronic angiotensin II-induced hypertension on cardiovascular hemodynamics and vascular properties in awake wild-type mice.

Main Methods:

  • Developed a novel experimental-computational workflow to bridge anesthetized and awake physiological states.
  • Utilized chronic angiotensin II infusion to induce hypertension in wild-type mice.
  • Compared hemodynamic and vascular property changes between hypertensive and normotensive groups under simulated awake conditions.

Main Results:

  • Anesthesia significantly impacted hemodynamics, particularly in angiotensin II-infused mice, leading to unexpected results when comparing anesthetized data.
  • Awake simulations revealed that angiotensin II infusion increased in vivo vascular stiffness in the descending thoracic and suprarenal abdominal aorta.
  • Hypertension led to increased pulse pressure in the distal aorta and characterized regionally varying vascular remodeling effects.

Conclusions:

  • The developed workflow accurately estimates in vivo cardiovascular conditions, overcoming anesthesia-induced artifacts.
  • Chronic angiotensin II infusion causes significant vascular remodeling and altered hemodynamics in mice, consistent with hypertension pathophysiology.
  • This approach enables a better characterization of hypertension's impact on vascular structure, properties, and hemodynamics in a mouse model.

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