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Hydrogen Sulfide and Polysulfides Mimic the Effects of Hypoxia in Bovine Pulmonary and Porcine Coronary Arteries
Author(s) -
Forgan Leonard George,
DeLeon Eric,
Gao Yan,
Whiteman Matt,
Olson Kenneth
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.1012.8
Subject(s) - hypoxia (environmental) , hydrogen sulfide , chemistry , coronary arteries , vascular smooth muscle , medicine , biochemistry , biophysics , oxygen , endocrinology , cardiology , anatomy , artery , biology , sulfur , smooth muscle , organic chemistry
The discovery of hydrogen sulfide (H 2 S) as an important biological signalling molecule has resulted in the elucidation of many complex biochemical and physiological functions of the molecule. One of its key physiological functions is the modulation of vascular tone. Our lab has shown potent effects of hypoxia on blood vessels from a wide range of craniates that is mimicked almost exactly by the application of exogenous H 2 S. Based on these data, we propose that H 2 S is a key transducer of hypoxia signalling and may be the elusive “oxygen sensor”. However, we hypothesise that some of the responses attributed to H 2 S may in fact be due to polysulfides (S n ) which form spontaneously upon dissolution. We hypothesised that vascular responses to H 2 S and polysulfides would mimic hypoxia responses in vascular smooth muscle. In the current study, we aimed to test this hypothesis by examining the effects of H 2 S, the mitochondrial H 2 S donor AP39 and polysulfides on isolated bovine pulmonary arteries and porcine coronary arteries. Paired vascular segments (with or without endothelium) were mounted inside Radnotti organ baths filled with Krebs‐Hanseleit Ringer (21% O 2 /5% CO 2 ; 37°C). Vascular responses were recorded in response to hypoxia (1%) or cumulative doses of H 2 S (Na 2 S), K 2 Sn, H 2 S 2 , H 2 S 3 , H 2 S 4 and AP39. Hypoxia caused a rapid and potent two‐phase constriction (50% of max) followed by dilation (25% of Max) of bovine pulmonary arteries. In contrast, hypoxia caused a small transient constriction (10% of max) followed by sustained dilation (30% of max) of porcine coronary arteries. Consistent with the effects of exogenous H 2 S application, K 2 S n , H 2 S 2 , H 2 S 3 , H 2 S 4 caused a constriction‐dilation in bovine pulmonary arteries of a similar magnitude to hypoxia responses. In contrast, AP39 caused a potent dilation only of pulmonary arteries. Application of all sulfides dilated porcine coronary arteries in a similar manner to hypoxia with responses also of a similar magnitude. Removal of the endothelium did not affect vascular responses in any preparation (P>0.05, F‐test). The current data support the hypothesis that H 2 S, and possibly polysulfides, act as an “oxygen‐sensor” in oxygen‐sensitive vessels since the physiological responses observed to hypoxia were mimicked by sulfide treatments. The data also suggest that polysulfides may be responsible for vasoactivity in response to exogenous H 2 S application. Future work will elucidate intracellular signalling events common to hypoxia and sulfide treatments on exposure to both H 2 S and polysulfides.