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C-reactive protein relaxes human vessels in vitro
Leonid Sternik1, Saquib Samee, Hartzel V Schaff
1Division of Cardiovascular Surgery, Mayo Clinic and the Mayo Foundation, Rochester, Minn 55905, USA.
Arteriosclerosis, Thrombosis, and Vascular Biology
|November 12, 2002
Summary
C-reactive protein (CRP) relaxes blood vessels independently of the endothelium. This vasorelaxation effect is mediated by potassium channels, suggesting CRP influences vascular tone.
Area of Science:
- Cardiovascular Biology
- Vascular Physiology
- Inflammation Research
Background:
- C-reactive protein (CRP) is a key inflammation marker and cardiovascular disease prognosticator.
- Emerging evidence indicates CRP possesses direct biological functions within the vascular wall.
Purpose of the Study:
- To investigate the vasoreactive properties of C-reactive protein (CRP).
- To elucidate the mechanisms underlying CRP-mediated vascular effects.
Main Methods:
- Human internal mammary artery rings were utilized in an organ bath setup.
- Vascular reactivity to CRP was assessed following precontraction with endothelin-1.
- Experiments involved interventions with potassium ions, potassium channel blockers (BaCl, tetraethylammonium chloride, glibenclamide), and a nitric oxide synthase inhibitor (N-monomethyl-L-arginine), as well as endothelium removal.
Main Results:
- CRP induced a dose-dependent relaxation of human internal mammary artery rings.
- This vasorelaxant effect was independent of endothelial function.
- CRP-induced relaxation was significantly attenuated by high potassium concentrations and specific potassium channel blockers (BaCl, tetraethylammonium chloride), but not by glibenclamide or nitric oxide synthase inhibition.
Conclusions:
- C-reactive protein (CRP) mediates an endothelium-independent vasorelaxation.
- The vasorelaxant effect of CRP is primarily mediated through potassium channels.
- CRP may play a role in the physiological regulation of vascular tone.