Endothelial Hyperpolarization in Humans
| Status: | Terminated |
|---|---|
| Conditions: | High Cholesterol |
| Therapuetic Areas: | Cardiology / Vascular Diseases |
| Healthy: | No |
| Age Range: | 21 - 65 |
| Updated: | 8/17/2018 |
| Start Date: | July 2002 |
| End Date: | January 2013 |
Physiology and Pathologic Role of Endothelium-Derived Hyperpolarizing Factor in Humans
The purpose of this study is to elucidate the role Endothelium-Derived Hyperpolarizing Factor
(EDHF) plays in dilating blood vessels and whether it differs between healthy people and
those with high cholesterol. A second purpose of the study is to determine the identity of
EDHF.
(EDHF) plays in dilating blood vessels and whether it differs between healthy people and
those with high cholesterol. A second purpose of the study is to determine the identity of
EDHF.
The vascular endothelium synthesizes at least four potent vasodilator substances: nitric
oxide (NO), prostacyclin, carbon monoxide and endothelium-derived hyperpolarizing factor
(EDHF) that contribute to vasodilator tone, and to inhibition of platelet activation and
inflammation. EDHF release is stimulated by receptor-dependent agonists such as acetylcholine
and bradykinin (BK), and leads to hyperpolarization of the underlying smooth muscle cells
presumably by opening Ca2+-activated K+ channels. Indirect pharmacological evidence suggests
that EDHF is a cytochrome P450-derived arachidonic acid metabolite, presumably an epoxide.
Although the pivotal role of NO to conduit vessel dilation in response to acute increases in
shear stress is well known, its' contribution to dilation with sustained increases in flow
are minimal, and may be due to EDHF release.
oxide (NO), prostacyclin, carbon monoxide and endothelium-derived hyperpolarizing factor
(EDHF) that contribute to vasodilator tone, and to inhibition of platelet activation and
inflammation. EDHF release is stimulated by receptor-dependent agonists such as acetylcholine
and bradykinin (BK), and leads to hyperpolarization of the underlying smooth muscle cells
presumably by opening Ca2+-activated K+ channels. Indirect pharmacological evidence suggests
that EDHF is a cytochrome P450-derived arachidonic acid metabolite, presumably an epoxide.
Although the pivotal role of NO to conduit vessel dilation in response to acute increases in
shear stress is well known, its' contribution to dilation with sustained increases in flow
are minimal, and may be due to EDHF release.
Inclusion Criteria:
- Hyperlipidemic (LDL > 140)
- Healthy Volunteer
Exclusion Criteria:
- Pregnancy
- Diabetes mellitus
- Cardiovascular Disease
- Hypertension
- Use of any regular medications
- Renal insufficiency
- Smoking (current or within the past 5 years)
- Bleeding disorder
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