Effects of carbon monoxide on sea lamprey and rainbow trout systemic arteries

Abstract

Carbon monoxide (CO) is an endogenously produced gas involved in vascular, neural, and inflammatory responses in mammals. CO activity in non‐mammalian vertebrates, however, is unknown. To this extent, we utilized smooth muscle myography to investigate the effects of exogenously applied CO (via CORM‐3) on isolated lamprey (Petromyzon marinus) dorsal aortas and trout (Oncorhynchus mykiss) efferent branchial (EBA) and celiacomesenteric (CMA) arteries. CORM dose‐dependently relaxed norepinephrine‐ (NE) and U46619‐, thromboxane‐A2 mimetic, ‐induced contractions of lamprey dorsal aortas. CORM relaxed both NE (10μM)‐and KCl (80mM)‐ prestimulated trout EBA and CMA dose dependently. EBA were 2‐fold more sensitive to CORM when prestimulated with NE than KCl and CORM relaxed 5‐fold more of the NE‐ than KCl‐induced tension. Glybenclamide (lOμM) inhibited a NE‐induced contraction, but did not effect a CORM induced relaxation. NS‐2028 (10μM), a solubule guanylyl cyclase inhibitor, had no effect on a NE‐contraction, but inhibited a subsequent CORM‐induced relaxation. Zinc protopophyrin‐IX (30μM), a heme‐oxygenase (HO) inhibitor, elicited a significant increase in baseline tension and eliminated the tri‐phasic EBA response to Na2S. These results implicate an active HO/CO pathway in trout vessels on resting vessel tonus and H2S‐induced vasoactivity that is partially mediated by soluble guanylyl cyclase.