Vasoactivity of hydrogen sulfide in normoxic and anoxic turtles (Trachemys scripta)

Stecyk JA, Skovgaard N, Nilsson GE, Wang T. Vasoactivity of hydrogen sulfide in normoxic and anoxic turtles (Trachemys scripta). Am J Physiol Regul Integr Comp Physiol 298: R1225-R1239, 2010. First published February 17, 2010; doi: 10.1152/ajpregu.00521.2009.-Systemic vascular resistance (R-sys) of freshwater turtles increases substantially during anoxia, but the underlying mechanisms are not fully understood. We investigated whether hydrogen sulfide (H2S), an endogenously produced metabolite believed to be an O-2 sensor/transducer of vasomotor tone, contributes to the increased Rsys of anoxic red-eared slider turtles (Trachemys scripta). Vascular infusion of the H2S donor NaHS in anesthetized turtles at 21 degrees C and fully recovered normoxic turtles at 5 degrees C and 21 degrees C revealed H2S to be a potent vasoconstrictor of the systemic circulation. Likewise, wire myography of isolated turtle mesenteric and pulmonary arteries demonstrated H2S to mediate an anoxia-induced constriction. Intriguingly, however, NaHS did not exert vasoconstrictory effects during anoxia (6 h at 21 degrees C; 14 days at 5 degrees C) when plasma H2S concentration, estimated from the colorimetric measurement of plasma acid-labile sulfide concentration, likely increased by similar to 3- and 4-fold during anoxia at 21 degrees C, and 5 degrees C, respectively. Yet, blockade of endogenous H2S production by DL-propargylglycine or hydroxylamine (0.44 mmol/kg) partially reversed the decreased systemic conductance (G(sys)) exhibited by 5 degrees C anoxic turtles. These findings suggest that the signal transduction pathway of H2S-mediated vasoactivity is either maximally activated in the systemic circulation of anoxic turtles and/or that it is oxygen dependent.