Norepinephrine vascoconstrictor escape in isolated meseneric arteries.
When isolated superfused cat mesentric arterial rings were exposed to norepinephrine(NE) 10'-6 g/ml, force initially increased but subsequently declined despite continuedadministration of NE.  Phasic contractions occurred in 48% of the vessels.  Norepinephrine concentrations just above threshold induced tonic contractions without escape.  When NE was administered after brief exposure of the arterial rings to low-calcium solutions, peak force development and escape were both reduced and phasic contractions were abolished.  Escape did not occur in potassium-depolarized vessels.  The peak response was increased and escape was reduced by substituting sodium in the Krebs solution by lithium and by substituting chloride with iodide or perchlorate.  Substitution of chloride by isethionate reduced the peak NE resonse and abolished escape.  Propanolol was without effect.  It is suggested that escape from NE vasoconstriction in mesenteric arteries is due to fading of propagated activity.
D000818:Animals; D002118:Calcium / Q000494:pharmacology; D002415:Cats; D002712:Chlorides / Q000494:pharmacology; D003250:Constriction; D066298:In Vitro Techniques; D007454:Iodides / Q000494:pharmacology; D007513:Isethionic Acid / Q000494:pharmacology; D008094:Lithium / Q000494:pharmacology; D008297:Male; D008638:Mesenteric Arteries / Q000187:drug effects*; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000187:drug effects; D009638:Norepinephrine / Q000494:pharmacology*; D010472:Perchlorates / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D012964:Sodium / Q000494:pharmacology; D014666:Vasomotor System / Q000187:drug effects*; D014700:Verapamil / Q000494:pharmacology
D002712:Chlorides; D007454:Iodides; D010472:Perchlorates; D007513:Isethionic Acid; D008094:Lithium; D012964:Sodium; D011433:Propranolol; D014700:Verapamil; D011188:Potassium; D002118:Calcium; D009638:Norepinephrine