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

Acute stress is a feature of our daily events that affects cardiovascular system and predisposes to hypertension. HS is now considered as a vasorelaxant gasotransmitter although it was considered as a toxic agent. In present work we studied the effect of HS releasing NaS in acute stress induced hypertension and cardiac damage. Rats were divided into five groups: control, NaS, acute stress, half dose of NaS (6  mg/kg), and finally full dose of NaS (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 HS. 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 enzymes 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 HS levels, RNA expression of CSE and SOD in cardiac tissues. NaS significantly decreased BP, serum levels of cortisol, cardiac enzymes markers, IL-6, and tissue levels of MDA. Also, NaS elevated serum HS, RNA expression of CSE, SOD in cardiac tissue and increased eNOs activity.