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RESEARCH PRODUCT

The Janus face of chlorogenic acid on vascular reactivity: A study on rat isolated vessels

Esther Ngo Lemba TomEsther Ngo Lemba TomCorine Girard-thernierC. Demougeot

subject

Maleendocrine systemCharybdotoxinEndotheliumPharmaceutical ScienceVasodilation030204 cardiovascular system & hematologyPharmacologyApaminMuscle Smooth Vascular03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDrug DiscoverymedicineAnimals[CHIM]Chemical SciencesRats WistarPhenylephrineAntihypertensive AgentsComputingMilieux_MISCELLANEOUSPharmacology[SDV.SP]Life Sciences [q-bio]/Pharmaceutical sciencesRatsVasodilationmedicine.anatomical_structureComplementary and alternative medicineBiochemistrychemistry030220 oncology & carcinogenesisHypertensionMolecular MedicineSodium nitroprussideEndothelium Vascularmedicine.symptomChlorogenic AcidVasoconstrictionAcetylcholinemedicine.drug

description

Abstract Background Chlorogenic acid (CGA), the main polyphenol contained in coffee, is a major contributor to dietary polyphenol intake. Few studies reported its anti-hypertensive properties but the mechanisms are still indefinite. Purpose The present study assessed the direct effect of CGA in endothelium denuded or intact aortic rings from male Wistar rats and the mechanisms involved. Methods/Results CGA induced a direct endothelium-dependent relaxation that was significantly reduced by L-NAME (10 −4  M), indomethacin (10 −5  M) and combination of apamin (10 −7  M) and charybdotoxin (10 −7  M). Incubation of rings with CGA induced a dual effect on agonist-induced vasorelaxation. At 10 −6  M, it enhanced the relaxant effects of acetylcholine and reduced the contracting effects of phenylephrine due to increased basal and stimulated NOS activity, respectively. At 10 −4  M, CGA blunted acetylcholine and bradykinin-induced vasorelaxation, reduced phenylephrine-induced vasoconstriction but did not change the response to sodium nitroprusside, a NO-donor. Conclusion In summary, CGA induces a direct endothelium-dependent vasodilation by increasing NOS, COX and EDHF signalling pathways. However, this new pharmacological action that can explain some positive effects of CGA in case of hypertension has to be modulated at the light of its deleterious impact on vascular relaxation at high concentrations and incite to be cautious when using high doses of CGA in clinical studies.

10.1016/j.phymed.2016.06.012https://hal-univ-fcomte.archives-ouvertes.fr/hal-03409012