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Updated: Sep 5, 2026

Measurement of Endothelium-Dependent Vasorelaxation in the Mouse Thoracic Aorta Using Tensometric Small Volume Chamber Myography
Published on: August 12, 2022
Chitosan and its subunits enhance adrenergic vasoconstriction and impair endothelium-dependent relaxation in rat
Saeedeh Pouri1, Marta Sanz-Gómez2, María S Fernández-Alfonso2
1Departamento de Química en Ciencias Farmacéuticas, Facultad de Farmacia, Universidad Complutense de Madrid, Plaza Ramón y Cajal S/N, Madrid, 28040, Spain; Instituto Pluridisciplinar, Universidad Complutense de Madrid, Paseo de Juan XXIII, n°1, Madrid, 28040, Spain.
Abstract:
Uncontrolled bleeding is a preventable cause of death in different scenarios. Chitosan (CS) is an attractive material for developing hemostatic products. Although vasoconstriction represents a critical first-line defense against blood loss, the effects of CS on vascular reactivity remain unexplored. In this work, the vascular response of two low-molecular-weight CS samples (crustacean and squid pen) is evaluated. Samples were characterized by UV-Vis, FTIR, GPC, and MALDI-TOF; viscosity, osmolality and cytotoxicity were also determined. Vascular responses were assessed in isolated rat aortic rings mounted in an organ bath. CS alone did not induce direct vasoconstriction. However, both CS samples increased vascular responsiveness by potentiating phenylephrine (PE)-induced contraction, while only crustacean CS significantly reduced the efficacy and potency of acetylcholine-mediated vasorelaxation. The CS monomers also enhanced PE-induced contraction, with glucosamine producing a stronger effect than N-acetylglucosamine. Although both samples had low degrees of acetylation, crustacean CS exerts a greater potentiating effect on α1-adrenergic contraction than squid pen CS, suggesting that factors other than degree of acetylation, i.e, molecular weight distribution, acetylation pattern, or polymer conformation, may contribute to the observed differences. This preliminary screening demonstrates that CS sensitizes the isolated rat aorta to adrenergic stimulation and reduces endothelial-dependent relaxation.
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