Effects of vasoactive agents on oxygen uptake in portal venous smooth muscle.
The studies concerned the effects of epinephrine, norepinephrine, phenylephrine, acetylcholine and K+ ions, in doses inducing maximal contraction on oxygen consumption of isolated rat portal veins. All the agonists tested stimulated the rate of O2 uptake, whereas high K+ did not. After specific blockade of alpha-adrenoceptors, the effects of epinephrine and norepinephrine on O2 consumption were not affected, whilst those of phenylephrine were abolished, and beta-adrenoceptor blockade suppressed the metabolic effect of epinephrine and norepinephrine. Acetylcholine was the agonist that most elevated O2 consumption; atropine blocked both contractile and metabolic effects of this drug. It appears that there is a clear dissociation between contractile and metabolic actions of some pharmacological agents, and a question is posed concerning phenylephrine and acetylcholine effects. Results with K+ suggest that different metabolic pathways might be involved in the activation and maintenance of drug-induced contraction in smooth muscle.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000502:physiology; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism*; D010101:Oxygen Consumption / Q000187:drug effects*; D011169:Portal Vein / Q000378:metabolism; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D013566:Sympathomimetics / Q000494:pharmacology
D013566:Sympathomimetics; D011189:Potassium Chloride; D000109:Acetylcholine; D002118:Calcium