Herein, we presented a review to show that the main mechanism underlying endothelial dysfunction is a decrease in the formation and bioavailability of NO against the background of inhibition of eNOS expression and reduced equivalents of the thiol-disulfide system with a simultaneous increase in the levels of cytotoxic forms of NO and the production of powerful vasoconstrictors. Based on the foregoing, the conjugated systems eNOS-L-arginine-NO/SH can be undoubtedly claimed in the near future as a promising target for the pharmacological correction of endothelial dysfunction. Since it is a nitrosative stress that plays the role in the development of endothelial dysfunction, it is topical to search for potential endothelial protectors in the series of S-substituted 1,2,4-triazole, which have the properties of antioxidanitts and NO scavengers. A striking representative of this cohort is Thiotriazolin which is a drug with cardioprotective, anti-ischemic and antioxidant properties, though does not possesses endothelial protective activity. As a result of chemical modification of the molecule of the latter, we obtained the compound (S)-2,6-diaminohexanoic acid 3-methyl-1,2,4-triazolyl-5-thioacetate (Angiolin), which manifests endothelium-protective properties against the background of cardio-protective, anti-ischemic and antioxidant activities.