Nervous control of circulation--the role of gasotransmitters, NO, CO, and H2S.
The origins and actions of gaseous signaling molecules, nitric oxide (NO), carbon monoxide (CO) and hydrogen sulfide (H(2)S) in the mammalian cardiovascular system have received considerable attention and it is evident that these three "gasotransmitters" perform a variety of homeostatic functions. The origins, actions and disposition of these gasotransmitters in the piscine vasculature are far from resolved. In most fish examined to date, NO or NO donors are generally in vitro and in vivo vasodilators acting via soluble guanylyl cyclase, although there is evidence for NO-mediated vasoconstriction. Injection of sodium nitroprusside into trout causes hypotension that is attributed to a reduction in systemic resistance. Unlike mammals, NO does not appear to have an endothelial origin in fish blood vessels as an endothelial NO synthase has not identified. However, neural NO synthase is prevalent in perivascular nerves and is the most likely source of NO for cardiovascular control in fish. CO is a vasodilator in lamprey and trout vessels, and it, like NO, appears to exert its action, at least in part, via guanylyl cyclase and potassium channel activation. Inhibition of CO production increases resting tone in trout vessels suggestive of tonic CO activity, but little else is known about the origin or control of CO in the fish vasculature. H(2)S is synthesized by fish vessels and its constrictory, dilatory, or even multi-phasic actions, are both species- and vessel-specific. A small component of H(2)S-mediated basal activity may be endothelial in origin, but to a large extent H(2)S affects vascular smooth muscle directly and the mechanisms are unclear. H(2)S injected into the dorsal aorta of unanesthetized trout often produces oscillations in arterial blood pressure suggestive of H(2)S activity in the central nervous system as well as peripheral vasculature. Collectively, these studies hint at significant involvement of the gasotransmitters in piscine cardiovascular function and hopefully provide a variety of avenues for future research.
Olson
Kenneth R
KR
Indiana University School of Medicine-South Bend, South Bend, IN 46617, USA. olson.1@nd.edu
Donald
John A
JA
D000818:Animals; D001341:Autonomic Nervous System / Q000502:physiology*; D001808:Blood Vessels / Q000294:innervation; D002248:Carbon Monoxide / Q000502:physiology; D002320:Cardiovascular Physiological Phenomena; D005399:Fishes / Q000502:physiology*; D006162:Guanylate Cyclase / Q000502:physiology; D006321:Heart / Q000294:innervation; D006862:Hydrogen Sulfide / Q000378:metabolism; D008322:Mammals; D009569:Nitric Oxide / Q000502:physiology; D014662:Vasoconstrictor Agents / Q000378:metabolism*; D014665:Vasodilator Agents / Q000378:metabolism*
D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009569:Nitric Oxide; D002248:Carbon Monoxide; D006162:Guanylate Cyclase; D006862:Hydrogen Sulfide