Abstract
Hydrogen sulfide (H2S) is an endogenous vasodilator in mammals, but its presence and function in other vertebrates is unknown. We generated H2S from NaHS and examined the effects on isolated efferent branchial arteries from steelhead (stEBA) or rainbow (rtEBA) trout. H 2S 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+ ATP 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 KC1 or K2SO4. stEBA phase 2 and phase 3 responses were dose dependent (EC50 = 1.1 ± 1.2 × 10-3 M and 6.7 ± 0.9 × 10-5 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 × 10-5 M, n = 4 (CM) and 3.8 ± 0.4 × 10-5 M, n = 9 (ISE); similar to phase 3 EC 50. Because NaHS has substantial vasoactive effects at physiological plasma concentrations, we propose that its soluble derivative, H2S, is a tonically active endogenous vasoregulator in trout.
| Original language | English (US) |
|---|---|
| Journal | American Journal of Physiology - Regulatory Integrative and Comparative Physiology |
| Volume | 286 |
| Issue number | 4 55-4 |
| State | Published - Apr 1 2004 |
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Keywords
- Cardiovascular
- Fish
- Guanosine 3′,5′-cyclic monophosphate
- Vasoconstrictor
- Vasodilator
ASJC Scopus subject areas
- Physiology
- Physiology (medical)
Cite this
Hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout. / Dombkowski, Ryan A.; Russell, Michael James; Olson, Kenneth R.
In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 286, No. 4 55-4, 01.04.2004.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Hydrogen sulfide as an endogenous regulator of vascular smooth muscle tone in trout
AU - Dombkowski, Ryan A.
AU - Russell, Michael James
AU - Olson, Kenneth R.
PY - 2004/4/1
Y1 - 2004/4/1
N2 - Hydrogen sulfide (H2S) is an endogenous vasodilator in mammals, but its presence and function in other vertebrates is unknown. We generated H2S from NaHS and examined the effects on isolated efferent branchial arteries from steelhead (stEBA) or rainbow (rtEBA) trout. H 2S 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+ ATP 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 KC1 or K2SO4. stEBA phase 2 and phase 3 responses were dose dependent (EC50 = 1.1 ± 1.2 × 10-3 M and 6.7 ± 0.9 × 10-5 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 × 10-5 M, n = 4 (CM) and 3.8 ± 0.4 × 10-5 M, n = 9 (ISE); similar to phase 3 EC 50. Because NaHS has substantial vasoactive effects at physiological plasma concentrations, we propose that its soluble derivative, H2S, is a tonically active endogenous vasoregulator in trout.
AB - Hydrogen sulfide (H2S) is an endogenous vasodilator in mammals, but its presence and function in other vertebrates is unknown. We generated H2S from NaHS and examined the effects on isolated efferent branchial arteries from steelhead (stEBA) or rainbow (rtEBA) trout. H 2S 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+ ATP 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 KC1 or K2SO4. stEBA phase 2 and phase 3 responses were dose dependent (EC50 = 1.1 ± 1.2 × 10-3 M and 6.7 ± 0.9 × 10-5 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 × 10-5 M, n = 4 (CM) and 3.8 ± 0.4 × 10-5 M, n = 9 (ISE); similar to phase 3 EC 50. Because NaHS has substantial vasoactive effects at physiological plasma concentrations, we propose that its soluble derivative, H2S, is a tonically active endogenous vasoregulator in trout.
KW - Cardiovascular
KW - Fish
KW - Guanosine 3′,5′-cyclic monophosphate
KW - Vasoconstrictor
KW - Vasodilator
UR - http://www.scopus.com/inward/record.url?scp=1642302470&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=1642302470&partnerID=8YFLogxK
M3 - Article
C2 - 15003943
AN - SCOPUS:1642302470
VL - 286
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
SN - 0363-6135
IS - 4 55-4
ER -