Effects of carbon monoxide on trout and lamprey vessels.
Carbon monoxide (CO) is endogenously produced by heme oxygenase (HO) and is involved in vascular, neural, and inflammatory responses in mammals. However, the biological activities of CO in nonmammalian vertebrates is unknown. To this extent, we used smooth muscle myography to investigate the effects of exogenously applied CO (delivered via a water-soluble CO-releasing molecule, CORM-3) on isolated lamprey (Petromyzon marinus) dorsal aortas and examined its mechanisms of action on trout (Oncorhynchus mykiss) efferent branchial (EBA) and celiacomesenteric (CMA) arteries. CORM-3 dose-dependently relaxed all vessels examined. Trout EBA were twofold more sensitive to CORM-3 when precontracted with norepinephrine (NE) than KCl and CORM-3 relaxed five-fold more of the NE- than KCl-induced tension. Glybenclamide (10 microM), an ATP-sensitive potassium channel inhibitor, inhibited NE-induced contraction, but did not affect CORM-3-induced relaxation. NS-2028 (10 microM), a soluble guanylyl cyclase inhibitor, had no effect on a NE-contraction, but inhibited a subsequent CORM-3-induced relaxation. Zinc protopophyrin-IX (ZnPP-IX, 0.3-30 microM), a HO inhibitor, elicited a small, yet dose-dependent and significant, increase in baseline tension but did not have any effect on subsequent NE-induced contractions or a nitric oxide-induced relaxation (via sodium nitroprusside). [ZnPP-IX] greater than 3 microM, however, significantly reduced the predominant vasodilatory response of trout EBA to hydrogen sulfide. These results implicate an active HO/CO pathway in trout vessels having an impact on resting vessel tone and CO-induced vasoactivity that is at least partially mediated by soluble guanylyl cyclase.
Dombkowski
Ryan A
RA
Department of Biology, Saint Mary's College, Notre Dame, Indiana, USA.
Whitfield
Nathan L
NL
Motterlini
Roberto
R
Gao
Yan
Y
Olson
Kenneth R
KR
D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000378:metabolism; D001934:Branchial Region / Q000098:blood supply; D002248:Carbon Monoxide / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005905:Glyburide / Q000494:pharmacology; D006162:Guanylate Cyclase / Q000037:antagonists & inhibitors / Q000378:metabolism; D006419:Heme Oxygenase (Decyclizing) / Q000037:antagonists & inhibitors / Q000378:metabolism; D006862:Hydrogen Sulfide / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000378:metabolism; D009213:Myography; D009569:Nitric Oxide / Q000378:metabolism; D009599:Nitroprusside / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D017686:Oncorhynchus mykiss / Q000378:metabolism*; D009942:Organometallic Compounds / Q000494:pharmacology*; D010069:Oxadiazoles / Q000494:pharmacology; D010078:Oxazines / Q000494:pharmacology; D048428:Petromyzon / Q000378:metabolism*; D011048:Polarography; D026902:Potassium Channel Blockers / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D011524:Protoporphyrins / Q000494:pharmacology; D018160:Receptors, Cytoplasmic and Nuclear / Q000037:antagonists & inhibitors / Q000378:metabolism; D000071756:Soluble Guanylyl Cyclase; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology*
D004791:Enzyme Inhibitors; C111257:NS 2028; D009942:Organometallic Compounds; D010069:Oxadiazoles; D010078:Oxazines; D026902:Potassium Channel Blockers; D011524:Protoporphyrins; D018160:Receptors, Cytoplasmic and Nuclear; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; C476530:tricarbonylchloro(glycinato)ruthenium(II); C017803:zinc protoporphyrin; D009599:Nitroprusside; D009569:Nitric Oxide; D011189:Potassium Chloride; D002248:Carbon Monoxide; D006419:Heme Oxygenase (Decyclizing); D006162:Guanylate Cyclase; D000071756:Soluble Guanylyl Cyclase; D005905:Glyburide; D009638:Norepinephrine; D006862:Hydrogen Sulfide