BACKGROUND: [corrected] Poly-N-acetylglucosamine (p-GlcNAc) is a secretion of marine diatoms that is known to be useful in controlling bleeding. As a component of promoting hemostasis, p-GlcNAc is thought to exert vasoconstrictor effects in arteries. The present study was undertaken to determine whether p-GlcNAc induced a significant vasoconstrictor effect and, if so, what the mechanism of this effect might be. MATERIALS AND METHODS: We examined vascular effects of p-GlcNAc on isolated aortic rings obtained from Sprague-Dawley rats. The rings were suspended in organ baths and precontracted with U46619, a thromboxane A2 mimetic. RESULTS: p-GlcNAc produced a concentration-dependent vasoconstriction over the range of 14 to 100 microg/ml. At a concentration of 100 microg/ml, p-GlcNAc significantly contracted aortic rings by 133 +/- 20 mg of developed force (P < 0.01). Neither a deacetylated derivative of p-GlcNAc nor a structurally related macromolecule, chitin, contracted rat aortic rings, indicating a specificity for p-GlcNAc. The vasoconstriction to p-GlcNAc was totally abolished in deendothelialized rat aortic rings, suggesting that an endothelial component is essential to the vasoconstriction. Pretreatment with the endothelin ET(A) receptor antagonist, JKC-301 (0.5 and 1 microM), significantly diminished p-GlcNAc-induced vasoconstriction by 57 to 61% (P < 0.01). However, p-GlcNAc did not significantly diminish nitric oxide release from rat aortic endothelium. CONCLUSION: These results provide evidence that p-GlcNAc significantly contracts isolated rat aortic rings via an endothelium-dependent mechanism, partly via enhancement of endothelin-1 release from endothelial cells. (c)2001 Elsevier Science.
BACKGROUND: [corrected] Poly-N-acetylglucosamine (p-GlcNAc) is a secretion of marine diatoms that is known to be useful in controlling bleeding. As a component of promoting hemostasis, p-GlcNAc is thought to exert vasoconstrictor effects in arteries. The present study was undertaken to determine whether p-GlcNAc induced a significant vasoconstrictor effect and, if so, what the mechanism of this effect might be. MATERIALS AND METHODS: We examined vascular effects of p-GlcNAc on isolated aortic rings obtained from Sprague-Dawley rats. The rings were suspended in organ baths and precontracted with U46619, a thromboxane A2 mimetic. RESULTS:p-GlcNAc produced a concentration-dependent vasoconstriction over the range of 14 to 100 microg/ml. At a concentration of 100 microg/ml, p-GlcNAc significantly contracted aortic rings by 133 +/- 20 mg of developed force (P < 0.01). Neither a deacetylated derivative of p-GlcNAc nor a structurally related macromolecule, chitin, contracted rat aortic rings, indicating a specificity for p-GlcNAc. The vasoconstriction to p-GlcNAc was totally abolished in deendothelialized rat aortic rings, suggesting that an endothelial component is essential to the vasoconstriction. Pretreatment with the endothelin ET(A) receptor antagonist, JKC-301 (0.5 and 1 microM), significantly diminished p-GlcNAc-induced vasoconstriction by 57 to 61% (P < 0.01). However, p-GlcNAc did not significantly diminish nitric oxide release from rat aortic endothelium. CONCLUSION: These results provide evidence that p-GlcNAc significantly contracts isolated rat aortic rings via an endothelium-dependent mechanism, partly via enhancement of endothelin-1 release from endothelial cells. (c)2001 Elsevier Science.