Vasoactivity of hydrogen sulfide in normoxic and anoxic turtles (Trachemys scripta).
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 (H(2)S), an endogenously produced metabolite believed to be an O(2) sensor/transducer of vasomotor tone, contributes to the increased R(sys) of anoxic red-eared slider turtles (Trachemys scripta). Vascular infusion of the H(2)S donor NaHS in anesthetized turtles at 21 degrees C and fully recovered normoxic turtles at 5 degrees C and 21 degrees C revealed H(2)S to be a potent vasoconstrictor of the systemic circulation. Likewise, wire myography of isolated turtle mesenteric and pulmonary arteries demonstrated H(2)S 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 H(2)S concentration, estimated from the colorimetric measurement of plasma acid-labile sulfide concentration, likely increased by approximately 3- and 4-fold during anoxia at 21 degrees C, and 5 degrees C, respectively. Yet, blockade of endogenous H(2)S 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 H(2)S-mediated vasoactivity is either maximally activated in the systemic circulation of anoxic turtles and/or that it is oxygen dependent.
Stecyk
Jonathan A W
JA
Physiology Programme, Department of Molecular Biosciences, University of Oslo, Oslo, Norway. jstecyk@ualberta.ca
Skovgaard
Nini
N
Nilsson
Göran E
GE
Wang
Tobias
T
D000480:Alkynes / Q000494:pharmacology; D000758:Anesthesia; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001831:Body Temperature / Q000502:physiology; D005260:Female; D005998:Glycine / Q000031:analogs & derivatives / Q000494:pharmacology; D006862:Hydrogen Sulfide / Q000097:blood / Q000494:pharmacology*; D019811:Hydroxylamine / Q000494:pharmacology; D000860:Hypoxia / Q000503:physiopathology*; D008297:Male; D008638:Mesenteric Arteries / Q000187:drug effects / Q000502:physiology; D010100:Oxygen / Q000494:pharmacology; D011651:Pulmonary Artery / Q000187:drug effects / Q000502:physiology; D013318:Stroke Volume / Q000187:drug effects / Q000502:physiology; D014426:Turtles / Q000502:physiology*; D014655:Vascular Resistance / Q000187:drug effects* / Q000502:physiology*; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology
D000480:Alkynes; D019811:Hydroxylamine; C009055:propargylglycine; D010100:Oxygen; D005998:Glycine; D006862:Hydrogen Sulfide