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

Abstract

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 (Rsys) 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 R sys of anoxic red-eared slider turtles (Trachemys scripta). Vascular infusion of the H 2S donor NaHS in anesthetized turtles at 21°C and fully recovered normoxic turtles at 5°C and 21°C revealed H 2S to be a potent vasoconstrictor of the systemic circulation. Likewise, wire myography of isolated turtle mesenteric and pulmonary arteries demonstrated H 2S to mediate an anoxia-induced constriction. Intriguingly, however, NaHS did not exert vasoconstrictory effects during anoxia (6 h at 21°C; 14 days at 5°C) when plasma H 2S concentration, estimated from the colorimetric measurement of plasma acid-labile sulfide concentration, likely increased by ϳ3-and 4-fold during anoxia at 21°C, and 5°C, respectively. Yet, blockade of endogenous H 2S production by DL-propargylglycine or hydroxylamine (0.44 mmol/kg) partially reversed the decreased systemic conductance (G sys) exhibited by 5°C anoxic turtles. These findings suggest that the signal transduction pathway of H 2S-mediated vasoactivity is either maximally activated in the systemic circulation of anoxic turtles and/or that it is oxygen dependent. red-eared slider; anoxia; temperature; cardiovascular; systemic resistance; pulmonary resistance; blood pressure; heart NORTH AMERICAN FRESHWATER turtles of the genera Trachemys, Chrysemys, and Chelydra exhibit a remarkable ability to survive a prolonged lack of oxygen (anoxia). At high temperatures (20 -25°C), these turtles successfully recover after 24 h of anoxia, but they can survive weeks to months without oxygen at the low temperatures, at which these animals overwinter (3-5°C) (57, 71). The exceptional anoxia tolerance is achieved through a profound reduction of whole animal metabolic rate, which slows metabolic fuel use and the rate of waste accumulation (21, 30) and the ability to use bone and shell as buffers to ameliorate the catastrophic acidosis that otherwise would accompany the sustained anaerobic metabolism (29,53).The large reduction in metabolism is attended by a pronounced lowering of cardiovascular performance during anoxia, where heart rate (f H ) and systemic blood flow (Q sys ) are drastically reduced and where pulmonary blood flow (Q pul ) virtually ceases (16,23,25,(65)(66)(67). While systemic blood pressure (P sys ) also decreases during anoxia, the reduction in Q sys is considerably larger, indicating a substantial (3-to 5-fold) increase in systemic peripheral resistance (R sys ). At high temperatures, the rise in R sys is largely due to increased ␣-adrenergic tone (54, 65), but ...

Circulating nitric oxide metabolites and cardiovascular changes in the turtleTrachemys scriptaduring normoxia, anoxia and reoxygenation

“…Consistent with previous studies on turtles, anoxia caused significant reductions in heart rate and systemic arterial pressure (Hicks and Wang, 1998;Stecyk et al, 2004;Overgaard et al, 2007). Although blood flow was not measured in the present study, earlier studies at a similar temperature have demonstrated a peripheral vasoconstriction mediated by increased sympathetic tone on the systemic vessels (Stecyk et al, 2004), and that H 2 S generation may play some role, particularly at low temperatures (Stecyk et al, 2010). Our study is the first to report on venous pressures in anoxic turtles.…”

Hydrogen sulfide and inflammation: the good, the bad, the ugly and the promising

“…While undoubtedly initially very useful pharmacological tools in a new but rapidly expanding research field, it is unlikely that these compounds are entirely specific since they target the pyridoxal phosphate (PLP) binding site of CSE and CBS [92] and other PLP-dependent and -independent enzymes (summarized in Table 1). This problem is exaggerated by the disparate concentration ranges commonly used in the laboratory (often used up to 10 mmol/l [93][94][95] …”

NO, CO and H2S: What about gasotransmitters in fish and amphibian heart?

“…The cardiovascular activity of H 2 S in poikilotherm vertebrates is weakly documented. The available data mainly concern its vasoactive properties that represent a conserved functional trait of this gasotransmitters, being present from fish to reptiles . In the classes so far examined, the gas elicits in vivo and in vitro vasoconstrictory, vasodilatory or multiphasic responses.…”