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Published on: May 14, 2020
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Ano1 mediates pressure-sensitive contraction frequency changes in mouse lymphatic collecting vessels
Scott D Zawieja1, Jorge A Castorena1, Peichun Gui1
1Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, MO.
The Journal of General Physiology
|March 14, 2019
Summary
Anoctamin 1 (Ano1) channels are crucial for lymphatic smooth muscle function. Loss of Ano1 impairs the pressure-frequency relationship in lymphatic vessels, impacting contractions.
Area of Science:
- Physiology
- Molecular Biology
- Cardiovascular Research
Background:
- Lymphatic collecting vessels contract spontaneously, with frequency dependent on pressure.
- Calcium-activated chloride channels (CaCCs) are hypothesized to initiate these contractions.
Purpose of the Study:
- To investigate the role of the canonical CaCC, Anoctamin 1 (Ano1, TMEM16a), in lymphatic smooth muscle pacemaking and pressure-dependent contractions.
Main Methods:
- Examined Ano1 expression in isolated murine lymphatic muscle cells.
- Measured CaCC currents and their inhibition by benzbromarone.
- Utilized Ano1-deficient mice (smooth muscle-specific deletion) and pharmacological inhibition.
- Assessed pressure-frequency relationships, membrane potential, and action potential characteristics in lymphatic vessels.
Main Results:
- Ano1 is expressed in murine lymphatic muscle cells, mediating functional CaCC currents.
- Ano1 deficiency (genetic or pharmacological) disrupts the pressure-frequency relationship.
- Loss of Ano1 leads to hyperpolarized membrane potential and reduced diastolic depolarization rate.
- Altered action potential shape, duration, and calcium transients were observed in Ano1-deficient vessels.
Conclusions:
- Ano1-mediated excitatory chloride current is critical for the pressure-sensitive contractile response of lymphatic vessels.
- Ano1 is a major component of the murine lymphatic action potential, regulating pacemaking and contractility.
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