Why the study?
Do arylthioamides act as H2S donors to induce vasorelaxation and reduce blood pressure in preclinical models?
Do arylthioamides act as H2S donors to induce vasorelaxation and reduce blood pressure in preclinical models?
Arylthioamides act as slow, l-cysteine-dependent H2S donors that induce vasorelaxation and reduce blood pressure in preclinical models, highlighting their potential for cardiovascular drug development.
Does not support clinical use; leaves open whether arylthioamides translate as H2S donors for hypertension.
A small library of arylthioamides 1-12 was easily synthesized, and their H2S-releasing properties were evaluated both in the absence or in the presence of an organic thiol such as l-cysteine. A number of arylthioamides (1-3 and 7) showed a slow and l-cysteine-dependent H2S-releasing mechanism, similar to that exhibited by the reference slow H2S-releasing agents, such as diallyl disulfide (DADS) and the phosphinodithioate derivative GYY 4137. Compound 1 strongly abolished the noradrenaline-induced vasoconstriction in isolated rat aortic rings and hyperpolarized the membranes of human vascular smooth muscle cells in a concentration-dependent fashion. Finally, a significant reduction of the systolic blood pressure of anesthetized normotensive rats was observed after its oral administration. Altogether these results highlighted the potential of arylthioamides 1-3 and 7 as H2S-donors for basic studies, and for the rational design/development of promising pharmacotherapeutic agents to treat cardiovascular diseases.
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Martelli et al. (2013) studied this question.
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