Possible Interaction: Acetylcholine and Homocysteine

“RESULTS Hc si gnificantly inhibited endothelium-dependent relaxation to ace tylcholine (A Ch) in a dose-dependent manner, and decreased cGMP levels increased by ACh in aorta.”

“ Homocysteine incubation impaired receptor-dependent and -independent endothelial function to ACh and A23187.”

“5 In conclusion, an acute infusion of homocysteine altered acetylcholine endothelium‐induced vasodilatation, whereas the adenosine vasodilatator effect was insensitive to the deleterious action of homocysteine in vitro.”

“ Homocysteine infusion for 30 min at a concentration of 200 μM or 2 mM abolished the endothelium‐dependent vasodilatation induced by acetylcholine (0.05 μM), but did not modify adenosine (1.5 μM)‐induced vasodilatation.”

“Microdissected renal interlobar arteries, which normally exhibit endothelium-derived hyperpolarizing factor-induced vasorelaxation, showed reduced nitric oxide synthase- and cyclooxygenase-independent vasorelaxation to acetylcholine after pretreatment with Hcy.”

“Homocysteine levels correlated with the pD2 values of acetylcholine among control and I/R groups, indicating that the increase in homocysteine was associated with decreased sensitivity to acetylcholine.”

“ tHcy negatively correlated with the ACh pD(2) values among control (r = -0.69; P < .05) and vehicle (r = -0.73; P < .05) groups, indicating that the increase in tHcy was associated with decreased sensitivity to ACh.”

“Incubation of pulmonary artery rings with Hcy (10(-3)M, 180min) resulted in significant inhibition of response to ACh (an endothelium-dependent vasodilator)(E(max): 55.3+/-6.7 vs. 13.1+/-2.0(*), P<0.05) while SNP (an endothelium-independent vasodilator)-induced relaxation was not changed significantly.”

“Exposure of aortic rings to homocysteine (0.3 ∼ 3 mmol/L) for 30 min induced a significant concentration-dependent inhibition of endothelium-dependent relaxation response to acetylcholine ( ACh ), but did not affect endothelium-independent relaxation response to sodium nitroprusside.”

“ Homocysteine inhibited not only the endothelial-derived NO as stimulated by ACh , but also the bioactivity of exogenously supplied NO by SNOHcy, SNOCys and SNP.”

“ Homocysteine (0.1 to 10 mmol/L) produced a significant (P<0.001) concentration- and time-dependent inhibition of endothelium-dependent relaxation in response to both acetylcholine and the calcium ionophore A23187.”