title: Agonist-induced tension determines vascular reactivity during anoxia and reoxygenation.
abstract: To determine the influence of pre-existing pharmacologically-induced tension on vascular reactivity during anoxia and reoxygenation, rat aortic rings were contracted with norepinephrine, epinephrine, endothelin or KCl to 1, 2 or 4 g of tension. The rings were then exposed to anoxia (95% N2) for 10 min followed by reoxygenation (95% O2). The degree of anoxia-mediated contraction varied with the magnitude of tension before anoxia and resembled the length-tension relationship in myocardial fibers. The optimal agonist-induced tension for maximal anoxic contraction was approximately 1 to 2 g. This relationship between tension and anoxic contraction was observed in all but KCl-contracted rings. The agonist- as well as KCl-contracted rings showed normal relaxant response to acetylcholine, suggesting that a decrease in endothelium-derived relaxing factor (EDRF) alone cannot be the basis of anoxic contraction and release of endothelium-derived constricting factors (EDCFs) may relate to anoxic contraction in agonist-preconstricted rings. The relationship between the magnitude of agonist-induced tension and the extent of anoxia-mediated contraction may relate to the ability of endothelium to release EDRF and EDCFs as well as to the degree of phosphorylation in vascular smooth muscle cells. The reoxygenation-mediated contraction was noted to progressively increase in all experiments regardless of the pharmacologic agent used. This increase in reoxygenation-mediated contraction correlated with pre-existing pharmacologic tension, and may relate to calcium influx and restoration of ATP and other mediators in the vascular tissues during reoxygenation.
authors.affiliation: Department of Medicine, University of Florida College of Medicine, Gainesville.
authors.forename: B C
authors.initials: BC
authors.lastname: Yang
authors.forename: W W
authors.initials: WW
authors.lastname: Nichols
authors.forename: D L
authors.initials: DL
authors.lastname: Lawson
authors.forename: J L
authors.initials: JL
authors.lastname: Mehta
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000502:physiology; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D016232:Endothelins / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology; D004837:Epinephrine / Q000494:pharmacology; D000860:Hypoxia / Q000503:physiopathology*; D066298:In Vitro Techniques; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology*; D009126:Muscle Relaxation / Q000187:drug effects / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000502:physiology; D009638:Norepinephrine / Q000494:pharmacology; D010100:Oxygen / Q000502:physiology*; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D015424:Reperfusion / Q000379:methods; D014662:Vasoconstrictor Agents / Q000494:pharmacology*; D019323:omega-N-Methylarginine
chemical_list: D016232:Endothelins; D014662:Vasoconstrictor Agents; D019323:omega-N-Methylarginine; D011189:Potassium Chloride; D001120:Arginine; D000109:Acetylcholine; D010100:Oxygen; D009638:Norepinephrine; D004837:Epinephrine