Related Experiment Video

Updated: Jun 12, 2026

Recording of Inward Rectifying K+ Currents in Freshly Isolated Basilar Artery Smooth Muscle Cells by Patch Clamp Technique
07:19

Recording of Inward Rectifying K+ Currents in Freshly Isolated Basilar Artery Smooth Muscle Cells by Patch Clamp Technique

Published on: February 7, 2025

Calcium-activated potassium channels - a therapeutic target for modulating nitric oxide in cardiovascular disease?

Thomas Dalsgaard1, Christel Kroigaard, Ulf Simonsen

  • 1Department of Pharmacology, Aarhus University, DK-8000 Aarhus C, Denmark. thomas.dalsgaard@farm.au.dk

Expert Opinion on Therapeutic Targets
|June 22, 2010
PubMed

Insights

Small (SK) and intermediate (IK) conductance calcium-activated potassium channels may treat endothelial dysfunction. Opening these channels boosts nitric oxide (NO) bioavailability and endothelium-dependent vasodilation, improving cardiovascular health.

Area of Science:

  • Cardiovascular research
  • Endothelial function
  • Ion channel pharmacology

Background:

  • Cardiovascular risk factors are linked to endothelial dysfunction, impacting vasodilation and nitric oxide (NO) bioavailability.
  • Endothelial dysfunction is a predictor of cardiovascular events.
  • Small (SK) and intermediate (IK) conductance Ca(2+)-activated K(+) channels are key in endothelium-dependent vasodilation.

Purpose of the Study:

  • To review the role of SK and IK channels in regulating NO bioavailability.
  • To explore SK and IK channels as potential therapeutic targets for endothelial dysfunction.

Main Methods:

  • Literature review focusing on SK and IK channel involvement in endothelial function.
  • Analysis of mechanisms linking channel activity to NO bioavailability and vasodilation.

Main Results:

  • SK and IK channels are involved in endothelium-derived hyperpolarizing factor (EDHF)-type vasodilation.
  • Channel activation enhances NO bioavailability via increased endothelial cell Ca(2+) influx, L-arginine uptake, and reduced reactive oxygen species (ROS) production.
  • This leads to increased endothelium-dependent vasodilation.

Conclusions:

  • Opening SK and IK channels promotes both EDHF and NO-mediated vasodilation.
  • SK and IK channel modulators show potential for improving endothelial cell function in cardiovascular disease.
Abstract

More Related Videos

Exploring Arterial Smooth Muscle Kv7 Potassium Channel Function using Patch Clamp Electrophysiology and Pressure Myography11:02

Exploring Arterial Smooth Muscle Kv7 Potassium Channel Function using Patch Clamp Electrophysiology and Pressure Myography

Published on: September 14, 2012

High-throughput Screening for Small-molecule Modulators of Inward Rectifier Potassium Channels10:07

High-throughput Screening for Small-molecule Modulators of Inward Rectifier Potassium Channels

Published on: January 27, 2013

Related Concept Videos

Antihypertensive Drugs: Action of Calcium Channel Blockers01:18

Antihypertensive Drugs: Action of Calcium Channel Blockers

Calcium ions are essential to contract smooth muscle cells in blood vessels. They enter these cells through voltage-dependent calcium channels, specifically L-type calcium channels in the cell membrane. These L-type calcium channels are integral to the excitation-contraction coupling process in smooth muscle. When a stimulus is received by smooth muscle cells, their membrane depolarizes. This alteration in membrane potential instigates the opening of L-type calcium channels. As a result,...
Nitric Oxide Signaling Pathway01:28

Nitric Oxide Signaling Pathway

Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure to...
Antianginal Drugs: Calcium Channel Blockers and Ranolazine01:25

Antianginal Drugs: Calcium Channel Blockers and Ranolazine

Angina pectoris, a primary symptom of ischemic heart disease, requires careful pharmacological interventions. In this context, calcium channel blockers (CCBs) and ranolazine have emerged as crucial pharmacotherapeutic agents, providing deep insights into the complexities of angina management.
CCBs, a diverse class that includes dihydropyridines (nifedipine) and diphenylalkylamines (verapamil and diltiazem), exert their effect by blocking calcium channels in cardiac and smooth muscle cells. This...
Antihypertensive Drugs: Vasodilators01:23

Antihypertensive Drugs: Vasodilators

Vasodilators, primarily affecting the smooth muscles within arterial and venous walls, are commonly used for hypertension treatment. Medications such as minoxidil and hydralazine primarily target arteries and arterioles, while sodium nitroprusside acts on arterioles and venules. Minoxidil, functioning as a prodrug, is metabolized by hepatic sulfotransferase into its active form, minoxidil sulfate, after oral administration. This metabolite binds to the sulfonylurea receptor (SUR) component of...
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
Antianginal Drugs: Nitrates and β-Blockers01:16

Antianginal Drugs: Nitrates and β-Blockers

In cardiovascular health, antianginal drugs combat angina pectoris — a condition marked by chest pain owing to diminished blood flow to the heart.
Organic nitrates,  such as nitroglycerin, play a pivotal role. Once metabolized, they liberate nitric oxide, a molecular marvel. Nitric oxide triggers guanylyl cyclase and augments cGMP production. This biochemical cascade orchestrates the relaxation of vascular smooth muscles, ushering in vasodilation and enhancing coronary blood flow. Administered...