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Hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout
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| Zeitschriftentitel: | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology |
|---|---|
| Personen und Körperschaften: | , , |
| In: | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 286, 2004, 4, S. R678-R685 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Physiological Society
|
| Schlagwörter: |
| author_facet |
Dombkowski, Ryan A. Russell, Michael J. Olson, Kenneth R. Dombkowski, Ryan A. Russell, Michael J. Olson, Kenneth R. |
|---|---|
| author |
Dombkowski, Ryan A. Russell, Michael J. Olson, Kenneth R. |
| spellingShingle |
Dombkowski, Ryan A. Russell, Michael J. Olson, Kenneth R. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout Physiology (medical) Physiology |
| author_sort |
dombkowski, ryan a. |
| spelling |
Dombkowski, Ryan A. Russell, Michael J. Olson, Kenneth R. 0363-6119 1522-1490 American Physiological Society Physiology (medical) Physiology http://dx.doi.org/10.1152/ajpregu.00419.2003 <jats:p> Hydrogen sulfide (H<jats:sub>2</jats:sub>S) is an endogenous vasodilator in mammals, but its presence and function in other vertebrates is unknown. We generated H<jats:sub>2</jats:sub>S from NaHS and examined the effects on isolated efferent branchial arteries from steelhead (stEBA) or rainbow (rtEBA) trout. H<jats:sub>2</jats:sub>S concentration was measured colorimetrically (CM) and with ion-selective electrodes (ISE) in rainbow trout plasma. NaHS produced a triphasic response consisting of a relaxation (phase 1), constriction (phase 2), and relaxation (phase 3) in both unstimulated vessels and in stEBA precontracted with carbachol (Carb). Phase 1 and phase 3 in stEBA were decreased and phase 2 increased in unstimulated vessels by K<jats:sup>+</jats:sup><jats:sub>ATP</jats:sub> channel inhibition (glibenclamide), or a cocktail of inhibitors of cyclooxygenase, lipoxygenase, and cytochrome P-450 (indomethacin, esculetin, and clotrimazole). Inhibition of soluble guanylate cyclase with ODQ or NS-2028 inhibited phase 3 in stEBA, although NaHS decreased cGMP production by rtEBA. stEBA phase 2 contractions were partially inhibited by the myosin light chain kinase inhibitor, ML-9, but unaffected by L-type calcium channel inhibition (methoxyverapamil), whereas contraction in rtEBA was partially inhibited by nifedipine or removal of extracellular calcium. Phase 3 relaxations were more pronounced in stEBA precontracted with Carb and norepinephrine (NE) than those contracted by KCl or K<jats:sub>2</jats:sub>SO<jats:sub>4</jats:sub>. stEBA phase 2 and phase 3 responses were dose dependent (EC<jats:sub>50</jats:sub> = 1.1 ± 1.2 × 10<jats:sup>-3</jats:sup> M and 6.7 ± 0.9 × 10<jats:sup>-5</jats:sup> M, respectively; n = 7). NaHS was also vasoactive in steelhead bulbus arteriosus, celiacomesenteric arteries, and anterior cardinal veins. Rainbow trout plasma sulfide concentration was 4.0 ± 0.3 × 10<jats:sup>-5</jats:sup> M, n = 4 (CM) and 3.8 ± 0.4 × 10<jats:sup>-5</jats:sup> M, n = 9 (ISE); similar to phase 3 EC<jats:sub>50</jats:sub>. Because NaHS has substantial vasoactive effects at physiological plasma concentrations, we propose that its soluble derivative, H<jats:sub>2</jats:sub>S, is a tonically active endogenous vasoregulator in trout. </jats:p> Hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout American Journal of Physiology-Regulatory, Integrative and Comparative Physiology |
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American Journal of Physiology-Regulatory, Integrative and Comparative Physiology |
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| title |
Hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout |
| title_unstemmed |
Hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout |
| title_full |
Hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout |
| title_fullStr |
Hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout |
| title_full_unstemmed |
Hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout |
| title_short |
Hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout |
| title_sort |
hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout |
| topic |
Physiology (medical) Physiology |
| url |
http://dx.doi.org/10.1152/ajpregu.00419.2003 |
| publishDate |
2004 |
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R678-R685 |
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<jats:p> Hydrogen sulfide (H<jats:sub>2</jats:sub>S) is an endogenous vasodilator in mammals, but its presence and function in other vertebrates is unknown. We generated H<jats:sub>2</jats:sub>S from NaHS and examined the effects on isolated efferent branchial arteries from steelhead (stEBA) or rainbow (rtEBA) trout. H<jats:sub>2</jats:sub>S concentration was measured colorimetrically (CM) and with ion-selective electrodes (ISE) in rainbow trout plasma. NaHS produced a triphasic response consisting of a relaxation (phase 1), constriction (phase 2), and relaxation (phase 3) in both unstimulated vessels and in stEBA precontracted with carbachol (Carb). Phase 1 and phase 3 in stEBA were decreased and phase 2 increased in unstimulated vessels by K<jats:sup>+</jats:sup><jats:sub>ATP</jats:sub> channel inhibition (glibenclamide), or a cocktail of inhibitors of cyclooxygenase, lipoxygenase, and cytochrome P-450 (indomethacin, esculetin, and clotrimazole). Inhibition of soluble guanylate cyclase with ODQ or NS-2028 inhibited phase 3 in stEBA, although NaHS decreased cGMP production by rtEBA. stEBA phase 2 contractions were partially inhibited by the myosin light chain kinase inhibitor, ML-9, but unaffected by L-type calcium channel inhibition (methoxyverapamil), whereas contraction in rtEBA was partially inhibited by nifedipine or removal of extracellular calcium. Phase 3 relaxations were more pronounced in stEBA precontracted with Carb and norepinephrine (NE) than those contracted by KCl or K<jats:sub>2</jats:sub>SO<jats:sub>4</jats:sub>. stEBA phase 2 and phase 3 responses were dose dependent (EC<jats:sub>50</jats:sub> = 1.1 ± 1.2 × 10<jats:sup>-3</jats:sup> M and 6.7 ± 0.9 × 10<jats:sup>-5</jats:sup> M, respectively; n = 7). NaHS was also vasoactive in steelhead bulbus arteriosus, celiacomesenteric arteries, and anterior cardinal veins. Rainbow trout plasma sulfide concentration was 4.0 ± 0.3 × 10<jats:sup>-5</jats:sup> M, n = 4 (CM) and 3.8 ± 0.4 × 10<jats:sup>-5</jats:sup> M, n = 9 (ISE); similar to phase 3 EC<jats:sub>50</jats:sub>. Because NaHS has substantial vasoactive effects at physiological plasma concentrations, we propose that its soluble derivative, H<jats:sub>2</jats:sub>S, is a tonically active endogenous vasoregulator in trout. </jats:p> |
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| description | <jats:p> Hydrogen sulfide (H<jats:sub>2</jats:sub>S) is an endogenous vasodilator in mammals, but its presence and function in other vertebrates is unknown. We generated H<jats:sub>2</jats:sub>S from NaHS and examined the effects on isolated efferent branchial arteries from steelhead (stEBA) or rainbow (rtEBA) trout. H<jats:sub>2</jats:sub>S concentration was measured colorimetrically (CM) and with ion-selective electrodes (ISE) in rainbow trout plasma. NaHS produced a triphasic response consisting of a relaxation (phase 1), constriction (phase 2), and relaxation (phase 3) in both unstimulated vessels and in stEBA precontracted with carbachol (Carb). Phase 1 and phase 3 in stEBA were decreased and phase 2 increased in unstimulated vessels by K<jats:sup>+</jats:sup><jats:sub>ATP</jats:sub> channel inhibition (glibenclamide), or a cocktail of inhibitors of cyclooxygenase, lipoxygenase, and cytochrome P-450 (indomethacin, esculetin, and clotrimazole). Inhibition of soluble guanylate cyclase with ODQ or NS-2028 inhibited phase 3 in stEBA, although NaHS decreased cGMP production by rtEBA. stEBA phase 2 contractions were partially inhibited by the myosin light chain kinase inhibitor, ML-9, but unaffected by L-type calcium channel inhibition (methoxyverapamil), whereas contraction in rtEBA was partially inhibited by nifedipine or removal of extracellular calcium. Phase 3 relaxations were more pronounced in stEBA precontracted with Carb and norepinephrine (NE) than those contracted by KCl or K<jats:sub>2</jats:sub>SO<jats:sub>4</jats:sub>. stEBA phase 2 and phase 3 responses were dose dependent (EC<jats:sub>50</jats:sub> = 1.1 ± 1.2 × 10<jats:sup>-3</jats:sup> M and 6.7 ± 0.9 × 10<jats:sup>-5</jats:sup> M, respectively; n = 7). NaHS was also vasoactive in steelhead bulbus arteriosus, celiacomesenteric arteries, and anterior cardinal veins. Rainbow trout plasma sulfide concentration was 4.0 ± 0.3 × 10<jats:sup>-5</jats:sup> M, n = 4 (CM) and 3.8 ± 0.4 × 10<jats:sup>-5</jats:sup> M, n = 9 (ISE); similar to phase 3 EC<jats:sub>50</jats:sub>. Because NaHS has substantial vasoactive effects at physiological plasma concentrations, we propose that its soluble derivative, H<jats:sub>2</jats:sub>S, is a tonically active endogenous vasoregulator in trout. </jats:p> |
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| institution | DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1 |
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| physical | R678-R685 |
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| spelling | Dombkowski, Ryan A. Russell, Michael J. Olson, Kenneth R. 0363-6119 1522-1490 American Physiological Society Physiology (medical) Physiology http://dx.doi.org/10.1152/ajpregu.00419.2003 <jats:p> Hydrogen sulfide (H<jats:sub>2</jats:sub>S) is an endogenous vasodilator in mammals, but its presence and function in other vertebrates is unknown. We generated H<jats:sub>2</jats:sub>S from NaHS and examined the effects on isolated efferent branchial arteries from steelhead (stEBA) or rainbow (rtEBA) trout. H<jats:sub>2</jats:sub>S concentration was measured colorimetrically (CM) and with ion-selective electrodes (ISE) in rainbow trout plasma. NaHS produced a triphasic response consisting of a relaxation (phase 1), constriction (phase 2), and relaxation (phase 3) in both unstimulated vessels and in stEBA precontracted with carbachol (Carb). Phase 1 and phase 3 in stEBA were decreased and phase 2 increased in unstimulated vessels by K<jats:sup>+</jats:sup><jats:sub>ATP</jats:sub> channel inhibition (glibenclamide), or a cocktail of inhibitors of cyclooxygenase, lipoxygenase, and cytochrome P-450 (indomethacin, esculetin, and clotrimazole). Inhibition of soluble guanylate cyclase with ODQ or NS-2028 inhibited phase 3 in stEBA, although NaHS decreased cGMP production by rtEBA. stEBA phase 2 contractions were partially inhibited by the myosin light chain kinase inhibitor, ML-9, but unaffected by L-type calcium channel inhibition (methoxyverapamil), whereas contraction in rtEBA was partially inhibited by nifedipine or removal of extracellular calcium. Phase 3 relaxations were more pronounced in stEBA precontracted with Carb and norepinephrine (NE) than those contracted by KCl or K<jats:sub>2</jats:sub>SO<jats:sub>4</jats:sub>. stEBA phase 2 and phase 3 responses were dose dependent (EC<jats:sub>50</jats:sub> = 1.1 ± 1.2 × 10<jats:sup>-3</jats:sup> M and 6.7 ± 0.9 × 10<jats:sup>-5</jats:sup> M, respectively; n = 7). NaHS was also vasoactive in steelhead bulbus arteriosus, celiacomesenteric arteries, and anterior cardinal veins. Rainbow trout plasma sulfide concentration was 4.0 ± 0.3 × 10<jats:sup>-5</jats:sup> M, n = 4 (CM) and 3.8 ± 0.4 × 10<jats:sup>-5</jats:sup> M, n = 9 (ISE); similar to phase 3 EC<jats:sub>50</jats:sub>. Because NaHS has substantial vasoactive effects at physiological plasma concentrations, we propose that its soluble derivative, H<jats:sub>2</jats:sub>S, is a tonically active endogenous vasoregulator in trout. </jats:p> Hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout American Journal of Physiology-Regulatory, Integrative and Comparative Physiology |
| spellingShingle | Dombkowski, Ryan A., Russell, Michael J., Olson, Kenneth R., American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout, Physiology (medical), Physiology |
| title | Hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout |
| title_full | Hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout |
| title_fullStr | Hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout |
| title_full_unstemmed | Hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout |
| title_short | Hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout |
| title_sort | hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout |
| title_unstemmed | Hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout |
| topic | Physiology (medical), Physiology |
| url | http://dx.doi.org/10.1152/ajpregu.00419.2003 |