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TMEM16A is implicated in the regulation of coronary flow and is altered in hypertension

Henry R Askew Page1,2, Thomas Dalsgaard2, Samuel N Baldwin1

  • 1Vascular Biology Research Centre, Institute of Molecular and Clinical Sciences, St George's University of London, London, UK.

British Journal of Pharmacology
|February 3, 2019
PubMed

Insights

Calcium-activated chloride channels, specifically TMEM16A, regulate coronary blood flow. This study found TMEM16A is increased in hypertensive rats, contributing to altered coronary artery function.

Area of Science:

  • Cardiovascular Physiology
  • Ion Channel Biology
  • Vascular Smooth Muscle Function

Background:

  • Coronary artery disease (CAD) necessitates understanding coronary blood flow regulation.
  • Calcium-activated chloride channels (CaCCs) influence arterial tone but their role in coronary arteries is unclear.
  • TMEM16A is the primary molecular component of CaCCs.

Purpose of the Study:

  • To investigate the expression and function of TMEM16A in rat coronary arteries.
  • To determine TMEM16A's role in regulating coronary blood flow and arterial tone.
  • To examine TMEM16A's involvement in altered coronary artery function in spontaneously hypertensive rats (SHRs).

Main Methods:

  • Performed mRNA and protein expression analysis.
  • Conducted electrophysiological studies on coronary artery myocytes.
  • Utilized novel TMEM16A inhibitors (MONNA, T16Ainh-A01, Ani9) for functional contractility and perfusion studies.
  • Assessed TMEM16A in coronary arteries from Wistar and spontaneously hypertensive rats (SHRs).

Main Results:

  • TMEM16A is expressed in rat coronary arteries.
  • TMEM16A inhibition (MONNA) caused hyperpolarization and attenuated 5-HT/U46619-induced contractions.
  • TMEM16A inhibitors increased coronary flow in isolated rat hearts.
  • TMEM16A mRNA was upregulated in SHRs, correlating with heightened sensitivity to vasoconstrictors.
  • MONNA reduced this enhanced sensitivity in SHRs.

Conclusions:

  • TMEM16A is a crucial regulator of coronary blood flow.
  • TMEM16A plays a significant role in the altered contractility observed in hypertensive rat coronary arteries.
  • TMEM16A represents a potential therapeutic target for managing hypertension-related cardiovascular complications.
Abstract

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