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Background Soluble guanylate cyclase (sGC) is the main receptor of nitric oxide (NO). NO binds to the ferrous heme moiety of sGC thus activating the enzyme and increasing cyclic GMP (cGMP) levels. sGC is inhibited by various oxidants which either convert ferrous heme to ferric suppressing NO binding or modify essential thiol groups of sGC. Certain heat shock proteins (Hsp) can protect the enzymes from this inactivation. Hence, we suggested that Hsp can block oxidant-induced inhibition of sGC.

Background Soluble guanylate cyclase (sGC) is a crucial enzyme at NO/cGMP-mediated vasodilation. There are NO-independent mechanisms of sGC activation besides wellknown enzyme activation by NO. Since 1966 oxatriazolium-5-olate derivatives are known as hypotensive agents at narcotized animals [1]. But the mechanism of their activity is not clarified. The goal of this research is to examine the ability of 3-(3-[1,2,4]triazolo)-oxatriazolium-5-olate (AS-6) to generate NO, to activate sGC, and to cause vasodilatation.