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Updated: Jan 12, 2026

Subcutaneous Angiotensin II Infusion using Osmotic Pumps Induces Aortic Aneurysms in Mice
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Smooth Muscle LRRC8A Knockout Preserves Vascular Function in Ang II Hypertension.

Hyehun Choi1, Sourav Panja1, Hong-Ngan Nguyen1

  • 1Department of Pediatrics, Vanderbilt University Medical Center, Nashville, TN.

Hypertension (Dallas, Tex. : 1979)
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Summary

Removing LRRC8A anion channels protects against Ang II-induced hypertension and vascular dysfunction. Knockout mice showed preserved vascular function and improved blood pressure dipping, indicating LRRC8A

Keywords:
angiotensin IIhypertensioninflammationmesenteric arteriessuperoxide

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Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Vascular Physiology

Background:

  • Angiotensin II (Ang II) induces hypertension and vascular inflammation via cytokines like TNFα.
  • In vascular smooth muscle cells (VSMCs), Ang II and TNFα activate NADPH oxidase 1 (Nox1) and associate with LRRC8A anion channels.
  • LRRC8A channels modulate inflammation and contractility in a RhoA-dependent manner, impacting vascular injury.

Purpose of the Study:

  • To investigate the role of LRRC8A anion channels in Ang II-induced hypertension and vascular dysfunction.
  • To determine if LRRC8A knockout preserves vascular function and reduces blood pressure in mice infused with Ang II.

Main Methods:

  • Wild-type and LRRC8A knockout mice underwent 14-day Ang II infusions.
  • Blood pressure was monitored via radiotelemetry.
  • Aortic and mesenteric artery function was assessed using wire myography, and VSMCs were isolated for analysis.

Main Results:

  • LRRC8A knockout mice exhibited preserved blood pressure dipping during inactive periods after Ang II infusion.
  • Vascular function in knockout mice was less impaired, with preserved relaxation to acetylcholine and reduced contraction to norepinephrine and serotonin.
  • Knockout vessels showed reduced proliferation (PCNA) and senescence induction by Ang II, alongside decreased Rho kinase activity markers.

Conclusions:

  • LRRC8A anion channels are critical mediators of VSMC inflammation and vascular dysfunction in Ang II-induced hypertension.
  • Targeting LRRC8A may offer a therapeutic strategy to preserve vascular function and improve blood pressure regulation in hypertensive conditions.