Role of nitric oxide and hydrogen sulfide from perivascular adipose tissue in vascular tone of resistant mesenteric arteries from endotoxemic rats

Endotoxin (lipopolysaccharide, LPS) administration can induce animals a sepsis-like syndrome, characterized by low blood pressure and vascular hyporeactivity to vasoconstrictor agents. The vascular hyporeactivity may be associated with the increase of nitric oxide (NO) and hydrogen sulfide (H 2 S). It has been shown that NO induces vasodilatation and H 2 S at lower concentrations ( 2 S released from PVAT may modulate the vascular tone in endotoxic rats. In this study, we examined the effect of PVAT on phenylephrine (PE, 10 −7 –10 −3  M)-induced vasocontraction of mesenteric artery rings from adult male Wistar rats at 1, 2, 4 and 6 h after LPS administration. In control rats, the PE-induced vasocontraction was increased by N w -nitro- l -arginine methyl ester (L-NAME) but was not affected by DL-propargylglycine (PPG, a cystathionine- γ -lyase inhibitor). The vascular hyporeactivity to PE is observed in the mesenteric artery obtained from all LPS groups. In early and late endotoxemia, the PE-induced vasocontraction was enhanced by L-NAME but reduced by PPG. However, the PE-induced vasocontraction was more enhanced by L-NAME in intact vessels compared with vessels without PVAT in late endotoxemia. Our results suggest that NO plays an important role in the regulation of vascular tone, whereas H 2 S could be important only in endotoxemia. In addition, NO released from PVAT may modulate the vascular tone in late endotoxemia.