KV channel trafficking and control of vascular tone

Raquibul Hasan, Jonathan Jaggar

Research output: Contribution to journalReview article

1 Citation (Scopus)

Abstract

Membrane potential is a principal regulator of arterial contractility. Arterial smooth muscle cells express several different types of ion channel that control membrane potential, including KV channels. KV channel activation leads to membrane hyperpolarization, resulting in inhibition of voltage-dependent Ca2+ channels, a reduction in [Ca2+]i, and vasodilation. In contrast, KV channel inhibition leads to membrane depolarization and vasoconstriction. The ability of KV channels to regulate arterial contractility is dependent upon the number of plasma membrane-resident channels and their open probability. Here, we will discuss mechanisms that alter the surface abundance of KV channel proteins in arterial smooth muscle cells and the functional consequences of such regulation. Cellular processes that will be described include those that modulate KV channel transcription, retrograde and anterograde trafficking, and protein degradation.

Original languageEnglish (US)
Article numbere12418
JournalMicrocirculation
Volume25
Issue number1
DOIs
StatePublished - Jan 1 2018

Fingerprint

Ion Channels
Membrane Potentials
Smooth Muscle Myocytes
Blood Vessels
Membranes
Vasoconstriction
Vasodilation
Proteolysis
Cell Membrane
Proteins

All Science Journal Classification (ASJC) codes

  • Physiology
  • Molecular Biology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

KV channel trafficking and control of vascular tone. / Hasan, Raquibul; Jaggar, Jonathan.

In: Microcirculation, Vol. 25, No. 1, e12418, 01.01.2018.

Research output: Contribution to journalReview article

@article{405d1e2bcf2545ac99af5cd3f3deb197,
title = "KV channel trafficking and control of vascular tone",
abstract = "Membrane potential is a principal regulator of arterial contractility. Arterial smooth muscle cells express several different types of ion channel that control membrane potential, including KV channels. KV channel activation leads to membrane hyperpolarization, resulting in inhibition of voltage-dependent Ca2+ channels, a reduction in [Ca2+]i, and vasodilation. In contrast, KV channel inhibition leads to membrane depolarization and vasoconstriction. The ability of KV channels to regulate arterial contractility is dependent upon the number of plasma membrane-resident channels and their open probability. Here, we will discuss mechanisms that alter the surface abundance of KV channel proteins in arterial smooth muscle cells and the functional consequences of such regulation. Cellular processes that will be described include those that modulate KV channel transcription, retrograde and anterograde trafficking, and protein degradation.",
author = "Raquibul Hasan and Jonathan Jaggar",
year = "2018",
month = "1",
day = "1",
doi = "10.1111/micc.12418",
language = "English (US)",
volume = "25",
journal = "Microcirculation",
issn = "1073-9688",
publisher = "Wiley-Blackwell",
number = "1",

}

TY - JOUR

T1 - KV channel trafficking and control of vascular tone

AU - Hasan, Raquibul

AU - Jaggar, Jonathan

PY - 2018/1/1

Y1 - 2018/1/1

N2 - Membrane potential is a principal regulator of arterial contractility. Arterial smooth muscle cells express several different types of ion channel that control membrane potential, including KV channels. KV channel activation leads to membrane hyperpolarization, resulting in inhibition of voltage-dependent Ca2+ channels, a reduction in [Ca2+]i, and vasodilation. In contrast, KV channel inhibition leads to membrane depolarization and vasoconstriction. The ability of KV channels to regulate arterial contractility is dependent upon the number of plasma membrane-resident channels and their open probability. Here, we will discuss mechanisms that alter the surface abundance of KV channel proteins in arterial smooth muscle cells and the functional consequences of such regulation. Cellular processes that will be described include those that modulate KV channel transcription, retrograde and anterograde trafficking, and protein degradation.

AB - Membrane potential is a principal regulator of arterial contractility. Arterial smooth muscle cells express several different types of ion channel that control membrane potential, including KV channels. KV channel activation leads to membrane hyperpolarization, resulting in inhibition of voltage-dependent Ca2+ channels, a reduction in [Ca2+]i, and vasodilation. In contrast, KV channel inhibition leads to membrane depolarization and vasoconstriction. The ability of KV channels to regulate arterial contractility is dependent upon the number of plasma membrane-resident channels and their open probability. Here, we will discuss mechanisms that alter the surface abundance of KV channel proteins in arterial smooth muscle cells and the functional consequences of such regulation. Cellular processes that will be described include those that modulate KV channel transcription, retrograde and anterograde trafficking, and protein degradation.

UR - http://www.scopus.com/inward/record.url?scp=85040238389&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85040238389&partnerID=8YFLogxK

U2 - 10.1111/micc.12418

DO - 10.1111/micc.12418

M3 - Review article

VL - 25

JO - Microcirculation

JF - Microcirculation

SN - 1073-9688

IS - 1

M1 - e12418

ER -