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Integrins mediate mechanical compression-induced endothelium-dependent vasodilation through endothelial nitric oxide
1Department of Biomedical Engineering, Department of Cellular and Integrative Physiology, Department of Surgery, and Indiana Center for Vascular Biology and Medicine, Indiana University-Purdue University Indianapolis, Indianapolis, IN 46202.
The Journal of General Physiology
|September 2, 2015
Summary
Muscle contraction compresses arterioles, causing vasodilation. Integrins mediate this process by enabling nitric oxide (NO) production in the endothelium, enhancing blood flow during exercise.
Area of Science:
- Cardiovascular Physiology
- Skeletal Muscle Physiology
- Endothelial Function
Background:
- Muscle contraction compresses intramuscular arterioles, leading to vasodilation and potentially enhanced blood flow.
- Endothelium-derived nitric oxide (NO) is implicated in this vasodilation, but the mechanism of NO production during arterial compression is unknown.
Purpose of the Study:
- To investigate the mechanism of nitric oxide (NO) production and vasodilation in response to cyclic arterial compression in swine myocardial and skeletal arterioles.
- To determine the role of endothelial integrins in mediating compression-induced vasodilation and NO production.
Main Methods:
- Isolated swine myocardial and skeletal arterioles were subjected to cyclic transmural pressure to simulate muscle contraction.
- Vasodilation was measured, and the effects of NO synthase inhibition, endothelium removal, and function-blocking integrin antibodies (α5β1, αvβ3) and RGD peptide were assessed.
- Endothelial and smooth muscle cell viability was confirmed using agonist-induced vasodilation.
Main Results:
- Cyclic pressure-induced vasodilation was dependent on changes in arteriole diameter and was attenuated by NO synthase inhibition and endothelium removal.
- Function-blocking antibodies against integrins α5β1 and αvβ3, as well as an RGD peptide, significantly reduced compression-induced vasodilation and NOx production.
- The vasodilation observed was smaller than that induced by direct pharmacological NO pathway activation.
Conclusions:
- Integrins play a crucial role in mediating endothelial nitric oxide (NO) production in response to cyclic arterial compression.
- This integrin-dependent NO production contributes to the vasodilation of small arteries under conditions simulating muscle activity.
- The findings elucidate a novel mechanism for regulating blood flow during muscle contraction.
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