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A Methodological Approach to Non-invasive Assessments of Vascular Function and Morphology
Published on: February 7, 2015
Contraction coupled endothelial nitric oxide release: a new paradigm for local vascular control?
1Department of Surgery, Brown University/The Miriam Hospital, 164 Summit Avenue, Providence, Rhode Island 02906, USA.
The Journal of Surgical Research
|August 23, 2001
Summary
Vascular contraction stimulates nitric oxide (NO) release in rat aorta, independent of central control. This finding reveals a local mechanism for blood vessel regulation.
Area of Science:
- Cardiovascular Physiology
- Endothelial Function
- Vascular Biology
Background:
- Nitric oxide (NO) is a key vasodilator in mammalian blood vessels.
- Its constitutive release is generally assumed.
- However, hemoglobin (Hb) induced contraction in precontracted rat aorta, suggesting NO release is stimulus-dependent.
Purpose of the Study:
- To investigate if vascular contraction triggers endothelial nitric oxide (NO) release.
- To explore the signaling pathways involved in this NO release.
Main Methods:
- Isolated rat thoracic aorta rings with/without endothelium were used.
- Vessels were contracted with various agonists.
- Nitric oxide (NO) release was assessed using a hemoglobin (Hb) contraction assay.
- Inhibition studies included nitro-l-arginine methyl ester (NAME) and gap junction inhibitors.
Main Results:
- Hemoglobin (Hb) induced significant additional contractions in precontracted aortic rings.
- This effect was abolished in endothelium-denuded or NAME-treated vessels.
- Contraction-coupled NO release was not inhibited by calmodulin or protein kinase inhibitors.
- Gap junction inhibition partially or fully blocked NE/Hb-mediated contractions.
Conclusions:
- Endothelial NO release is coupled to contractile stimuli in the rat thoracic aorta.
- This suggests a local vascular control mechanism distinct from central regulation.
- The pathway may involve mechanisms other than the canonical Ca(2+)-calmodulin-dependent endothelial NO synthase.
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