Although down-regulation of Arap1 during endotoxemia appears to be relevant for the development of hypotension and, by inference, hyporesponsiveness to angiotensin II, it should be noted that other mechanisms, such as inadequate formation of vasodilator agents and resistance to other vasoconstrictors, are relevant in the pathogenesis of septic circulatory failure [1]. This evidence concerns the gene ARAP1 and serum lipopolysaccharide activity.