H2S releasing Sodium sulfide protects from acute stress-induced hypertension by increasing the activity of endothelial nitric oxide synthase enzyme.

Abstract Acute stress is a feature of our daily events that affects cardiovascular system and predisposes to hypertension. H2S is now considered as a vasorelaxant gasotransmitter although it was considered as a toxic agent. In present work we studied the effect of H2S releasing Na2S in acute stress induced hypertension and cardiac damage. Rats were divided into five groups: control, Na2S, acute stress, half dose of Na2S (6 mg/kg), and finally full dose of Na2S (12 mg/kg) to acute stressed rats. BP was measured then blood samples were taken for estimation of cortisol, cardiac enzymes markers, IL-6 and H2S. Finally, animals were sacrificed, hearts and thoracic aortae were excised for histological assessment, estimation of MDA, SOD and RNA extraction of CSE. Acute stress significantly elevated BP, cortisol, cardiac enzyme markers, IL-6, and tissue levels of MDA. It also, induced cardiac cell damage with congested B.V., extravasation of blood and decreased eNOs. Moreover, acute stress reduced H2S levels, RNA expression of CSE and SOD in cardiac tissues. Na2S significantly decreased BP, serum levels of cortisol, cardiac enzyme markers, IL-6, and tissue levels of MDA. Also, Na2S elevated serum H2S, RNA expression of CSE, SOD in cardiac tissue and increased eNOs activity.