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First published online June 27, 2008
Journal of Experimental Biology 211, 2205-2213 (2008)
Published by The Company of Biologists 2008
doi: 10.1242/jeb.016766

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Oxygen dependency of hydrogen sulfide-mediated vasoconstriction in cyclostome aortas

Kenneth R. Olson^1,*, Leonard G. Forgan², Ryan A. Dombkowski³ and Malcolm E. Forster²

¹ Indiana University School of Medicine–South Bend, 1234 Notre Dame Avenue, South Bend, IN 46617, USA
² School of Biological Sciences, University of Canterbury, Private Bag 4800, Christchurch 8020, New Zealand
³ Department of Biology, Saint Mary's College, Notre Dame, IN 46556, USA

View larger version (4K): [in this window] [in a new window]   Fig. 1. Cumulative carbachol dose–response curve for efferent branchial arteries (mean ± s.e.m.; N=4).

View larger version (7K): [in this window] [in a new window]   Fig. 2. Effects of H2S (administered as Na2S) on buffer pH (open circles, N=2) and contraction of dorsal aortas (filled circles, N=4). pH is relatively stable at an [H2S] of1 mmol l–1, but higher concentrations produce increasing alkalinity and appear to augment aortic contraction.

View larger version (10K): [in this window] [in a new window]   Fig. 3. (A) H2S dose–response curves for hagfish dorsal aortas (filled circles; N=22) and efferent branchial arteries (filled triangles; N=8) bubbled with room air, and dorsal aortas bubbled with 100% nitrogen (open circles; N=10). Aortas bubbled with nitrogen were significantly (*) more sensitive to low concentrations of H2S than air-bubbled aortas and appear to have a two-phase response to H2S. H2S at 100 and 300 µmol l–1 produces a significantly greater response in normoxic efferent branchial arteries than normoxic dorsal aortas (). (B) H2S dose–response curves for lamprey dorsal aortas bubbled with room air (filled circles; N=8) or during moderate hypoxia (open circles; N=8). Hypoxic vessels were significantly (*) more sensitive to H2S. Values are means ± s.e.m.

View larger version (9K): [in this window] [in a new window]   Fig. 4. Effects of (A) L-cysteine, the substrate for H2S synthesis, (B) the cystathionine β-synthase inhibitor, amino-oxyacetate (AOA), (C) the cystathionine -lyase inhibitor, propargyl glycine (PPG) and (D) an uncoupler of pyridoxyl 5'-phosphate-dependent enzymes, hydroxylamine (HA) on hypoxic (100% N2) vasoconstriction of hagfish dorsal aorta. Vessels were continuously contracted with N2 then given cumulative additions of cysteine or inhibitors followed by 10 µmol l–1 carbachol (CBC). Values are expressed as the average tension (mean ± s.e.m.) as the percentage of the reference carbachol contraction (100%; dashed line). Hypoxic contractions (N2) were generally 30% of the reference carbachol contraction. Cysteine at 1 mmol l–1 approximately doubled the force of the original N2 contraction, whereas raising cysteine to 10 mmol l–1 relaxed the vessels back to the original N2 level (* significant increase from N2; significant decrease from 1 mmol l–1 cysteine; N=7). Hypoxic contractions were unaffected by 100 µmol l–1 and 1 mmol l–1 AOA. At 4 mmol l–1 AOA, the hypoxic contraction was completely inhibited (*; N=8). PPG did not significantly affect the N2 contraction (N=8). HA, 10 µmol l–1 HA significantly (*) increased the force of the N2 contraction and tension was maintained at 100 µmol l–1 and 1 mmol l–1 (N=8).

View larger version (10K): [in this window] [in a new window]   Fig. 5. Effect of PO2 on oxygen consumption (O2) by hagfish dorsal aortas (A) and salmon vessels (B). O2 is tightly regulated in unstimulated hagfish aortas (filled triangles) between a PO2 of 15 and 115 mmHg (1 mmHg=0.133 kPa), but varies with PO2 at either extreme. At a PO2 of 12 mmHg O2 falls to 90% of the regulated level and O2 is halved at 3 mmHg (P50). O2 was not affected by pre-contracting hagfish aortas with 100 µmol l–1 carbachol (CBC; open triangles). O2 was also regulated in unstimulated salmon vessels (B; filled circles) between a PO2 of 15 and 115 mmHg; however, per unit tissue mass it was five times greater than that of hagfish aortas. Pre-treatment of salmon vessels with 100 µmol l–1 carbachol nearly doubled O2 at all PO2 (open circles). Mean ± s.e.m.; N indicates the number of groups of 4–6 vessels per group in each experiment (standard error not shown when within the symbol). Broken line shows the PO2 dependency of hypoxic contraction in hagfish dorsal aortas [redrawn from Olson et al. (Olson et al., 2001)].

View larger version (16K): [in this window] [in a new window]   Fig. 6. Effect of (A) H2S (as Na2S), (B) the substrate for H2S synthesis, L-cysteine (cysteine), and inhibitors of H2S production, (C) amino-oxyacetate (AOA) and (D) hydroxylamine (HA), on oxygen consumption (O2) by hagfish dorsal aortas. O2 was stimulated by 10 µmol l–1 H2S and 10 mmol l–1 cysteine and inhibited by 100 µmol l–1 and 1 mmol l–1 H2S and by 10 mmol l–1 AOA and 10 mmol l–1 HA. Carbachol (100 µmol l–1) pre-treatment (+CBC) did not affect O2 at any [H2S] compared to untreated (–CBC) vessels, although O2 was significantly different between 10 µmol l–1 and 100 µmol l–1 H2S in carbachol pretreated vessels. Mean + s.e.m.; N=7 (H2S), 5 (cysteine), 4 (AOA), 4 (HA) groups of 4–6 vessels per group; *significantly different from respective control; significantly different from +CBC control.

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