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Chloride ion currents contribute functionally to norepinephrine-induced vascular contraction

F S Lamb¹, T J Barna

¹Department of Pediatrics, University of Iowa, Iowa City, Iowa, 52242, USA.

The American Journal of Physiology

|August 5, 1998

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Chloride currents are crucial for vascular smooth muscle contraction. Inhibiting these currents significantly alters norepinephrine-induced responses, highlighting their role in regulating blood vessel tone.

Area of Science:

Physiology
Vascular Biology
Ion Transport

Background:

Norepinephrine (NE) stimulates chloride (Cl-) efflux in vascular smooth muscle (VSM) cells, leading to membrane depolarization.
The role of Cl- currents in agonist-induced VSM contraction remains incompletely understood.

Purpose of the Study:

To investigate the critical role of cellular Cl- handling in agonist-induced VSM contractility.
To determine if interfering with Cl- currents affects VSM contraction.

Main Methods:

Isometric contraction of rat aortic rings was measured in various buffer conditions.
Extracellular Cl- was substituted with methanesulfonate (MS), iodide (I-), or bromide (Br-).
The effects of Cl- transport inhibitors (bumetanide), Cl--channel blockers (DIDS, anthracene-9-carboxylic acid, niflumic acid), and sarcoplasmic reticulum modulators (cyclopiazonic acid, ryanodine) were assessed.

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Main Results:

Low extracellular Cl- potentiated NE- and serotonin-induced contractions but did not affect KCl or Ca2+-independent NE responses.
Substitution with I- or Br- suppressed NE-induced contractions.
Inhibitors of Cl- transport and Cl--channels significantly reduced NE-induced contraction.
Disruption of sarcoplasmic reticular function abolished the potentiation of NE response in low-Cl- buffer.

Conclusions:

A Cl- current with a specific permeability sequence (I- > Br- > Cl- > MS) is essential for agonist-induced VSM contraction.
Cellular Cl- handling plays a critical role in regulating vascular smooth muscle contractility.