Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Paracrine Signaling01:21

Paracrine Signaling

60.4K
Paracrine signaling allows cells to communicate with their immediate neighbors via secretion of signaling molecules. Such a signal can only trigger a response in nearby target cells because the signal molecules degrade quickly or are inactivated if not taken up. Prominent examples of paracrine signaling include nitric oxide signaling in blood vessels, synaptic signaling of neurons, the blood clotting system, tissue repair/wound healing, and local allergic skin reactions. Nitric oxide as a...
60.4K
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

3.9K
Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
3.9K
Endocrine Signaling01:45

Endocrine Signaling

69.3K
Endocrine cells produce hormones to communicate with remote target cells found in other organs. The hormone reaches these distant areas using the circulatory system. This exposes the whole organism to the hormone but only those cells expressing hormone receptors or target cells are affected. Thus, endocrine signaling induces slow responses from its target cells but these effects also last longer.
69.3K
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

3.8K
Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
3.8K
Nitric Oxide Signaling Pathway01:28

Nitric Oxide Signaling Pathway

6.7K
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...
6.7K
G-Protein Gated Ion Channels01:21

G-Protein Gated Ion Channels

6.9K
GPCRs are primarily responsible for our sense of smell, taste, and vision.  The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
Sensory...
6.9K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Conducted dilatation to ATP and K<sup>+</sup> in rat skeletal muscle arterioles.

Acta physiologica (Oxford, England)·2016
Same author

TRPM4 inhibitor 9-phenanthrol activates endothelial cell intermediate conductance calcium-activated potassium channels in rat isolated mesenteric artery.

British journal of pharmacology·2014
Same author

β₁-Adrenoceptor stimulation suppresses endothelial IK(Ca)-channel hyperpolarization and associated dilatation in resistance arteries.

British journal of pharmacology·2013
Same author

The vascular endothelium: still amazing us 30 years on.

British journal of pharmacology·2011
Same author

Vascular hyperpolarization to β-adrenoceptor agonists evokes spreading dilatation in rat isolated mesenteric arteries.

British journal of pharmacology·2011
Same author

Evidence both L-type and non-L-type voltage-dependent calcium channels contribute to cerebral artery vasospasm following loss of NO in the rat.

Vascular pharmacology·2010

Related Experiment Video

Updated: Mar 27, 2026

Isolation of Microvascular Endothelial Tubes from Mouse Resistance Arteries
09:23

Isolation of Microvascular Endothelial Tubes from Mouse Resistance Arteries

Published on: November 25, 2013

16.2K

EDH: endothelium-dependent hyperpolarization and microvascular signalling.

C J Garland1, K A Dora1

  • 1Department of Pharmacology, University of Oxford, Oxford, UK.

Acta Physiologica (Oxford, England)
|January 12, 2016
PubMed
Summary

Endothelium-dependent hyperpolarization (EDH) involves calcium-activated potassium channels in endothelial cells, leading to vasodilation. This process modulates blood pressure and flow, with conducted vasodilation playing a key role in microcirculation.

Keywords:
IKC aSKC aKCa2.3KCa3.1connexinsgap-junctionsvasodilatation

More Related Videos

Author Spotlight: A Pharmacodissection Approach to Uncover Mechanisms in Cardiovascular Disease Risk Populations
08:21

Author Spotlight: A Pharmacodissection Approach to Uncover Mechanisms in Cardiovascular Disease Risk Populations

Published on: July 21, 2023

2.2K
Development and Characterization of In Vitro Microvessel Network and Quantitative Measurements of Endothelial [Ca2+]i and Nitric Oxide Production
09:39

Development and Characterization of In Vitro Microvessel Network and Quantitative Measurements of Endothelial [Ca2+]i and Nitric Oxide Production

Published on: May 19, 2016

9.2K

Related Experiment Videos

Last Updated: Mar 27, 2026

Isolation of Microvascular Endothelial Tubes from Mouse Resistance Arteries
09:23

Isolation of Microvascular Endothelial Tubes from Mouse Resistance Arteries

Published on: November 25, 2013

16.2K
Author Spotlight: A Pharmacodissection Approach to Uncover Mechanisms in Cardiovascular Disease Risk Populations
08:21

Author Spotlight: A Pharmacodissection Approach to Uncover Mechanisms in Cardiovascular Disease Risk Populations

Published on: July 21, 2023

2.2K
Development and Characterization of In Vitro Microvessel Network and Quantitative Measurements of Endothelial [Ca2+]i and Nitric Oxide Production
09:39

Development and Characterization of In Vitro Microvessel Network and Quantitative Measurements of Endothelial [Ca2+]i and Nitric Oxide Production

Published on: May 19, 2016

9.2K

Area of Science:

  • Vascular Physiology
  • Cardiovascular Research
  • Cellular Signaling

Background:

  • Endothelium-dependent hyperpolarizing factor (EDHF) is crucial for regulating blood pressure and flow in small arteries.
  • The concept has evolved from a diffusible factor to endothelium-dependent hyperpolarization (EDH), involving current spread.

Purpose of the Study:

  • To elucidate the mechanisms of EDH and its role in vascular smooth muscle (VSM) hyperpolarization and vasodilation.
  • To identify the specific calcium-sensitive potassium channels involved in the EDH pathway.

Main Methods:

  • Investigated EDH responses using pharmacological blockers of potassium channels (apamin, charybdotoxin, iberiotoxin).
  • Examined the localization of SKCa and IKCa channels in endothelial microdomains and their role in current spread.
  • Studied the contribution of K+ efflux and myoendothelial gap junctions to EDH.

Main Results:

  • EDH is activated by increased endothelial intracellular calcium, stimulating SKCa and IKCa channels.
  • Apamin and charybdotoxin, but not iberiotoxin, blocked EDH responses, identifying SKCa and IKCa as key channels.
  • K+ efflux and conducted hyperpolarization via gap junctions contribute to VSM hyperpolarization and conducted vasodilatation (CVD).

Conclusions:

  • EDH involves both diffusible K+ and electrical current spread through myoendothelial gap junctions.
  • SKCa and IKCa channels are critical for EDH, influencing vasodilation and blood flow regulation.
  • The sustained mechanisms of conducted hyperpolarization in arteries remain an area for further investigation.