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Assessing Myogenic Response and Vasoactivity In Resistance Mesenteric Arteries Using Pressure Myography
Published on: July 6, 2015
Elevated pressure selectively blunts flow-evoked vasodilatation in rat mesenteric small arteries
F H Christensen1, T Hansen, E Stankevicius
1Department of Pharmacology, University of Aarhus, 8000 Aarhus C, Denmark.
British Journal of Pharmacology
|November 28, 2006
Summary
Elevated intraluminal pressure impairs nitric oxide-mediated vasodilation in rat arteries, likely via endothelin receptors and superoxide. Acetylcholine-induced vasodilation remained unaffected, suggesting pressure affects specific pathways.
Area of Science:
- Vascular Physiology
- Endothelium Function
- Cardiovascular Research
Background:
- Endothelium-dependent vasodilation is crucial for blood flow regulation.
- Intraluminal pressure changes can influence vascular function.
- Mechanisms of pressure-induced vasodilation impairment require further investigation.
Purpose of the Study:
- To investigate the mechanisms of impaired endothelium-dependent vasodilation caused by elevated intraluminal pressure.
- To determine the specific pathways affected by transient pressure increases in rat mesenteric small arteries.
Main Methods:
- Rat mesenteric small arteries were studied using a pressure myograph.
- Arteries were subjected to elevated intraluminal pressure (50 to 120 mmHg) for 1 hour.
- Endothelium-dependent vasodilation was assessed using various pharmacological agents and flow-induced responses.
Main Results:
- Elevated pressure inhibited nitric oxide (NO)-mediated, flow-evoked vasodilation.
- This inhibition was linked to increased superoxide formation and endothelin receptor activation.
- Acetylcholine-induced vasodilation, mediated by endothelium-derived hyperpolarizing factor, was not affected.
Conclusions:
- Transient elevated intraluminal pressure selectively impairs NO-mediated vasodilation.
- Endothelin receptor activation and superoxide production are likely key mediators.
- Pressure elevation does not impact endothelium-derived hyperpolarizing factor-mediated vasodilation in these arteries.
