Roles of noradrenaline and ATP in sympathetic vasoconstriction of the guinea-pig main ear artery.
This study has investigated the roles of noradrenaline (NA) and adenosine 5'-triphosphate (ATP) in sympathetic vasoconstriction of the main ear artery from guinea-pigs. A range of agents which interact with adrenoceptors or purinoceptors was tested on contractions produced by exogenous NA or ATP, and on contractions produced by transmural stimulation of sympathetic axons. Contractions produced by NA were antagonized competitively by prazosin (Schild plot slope 0.88 +/- 0.13, not significantly different from 1.0). Dihydroergotamine (10 microM) produced significant depression of contractions produced by all concentrations of NA. Yohimbine (1 microM) caused a small rightward shift in the NA concentration-response curves (0.34 log units), whereas propranolol had no effect. alpha,beta,m-ATP (6 microM) enhanced contractions produced by low concentrations of NA (0.1-1 microM), whereas suramin (30 microM) produced a slight depression in the maximum NA-induced contraction in all experiments. Contractions produced by ATP (0.1 mM) were greatly reduced by suramin (30 microM; 59% reduction) and by alpha,beta,m-ATP (6 microM); 96% reduction), and were slightly depressed by dihydroergotamine (10 microM; 12% reduction). Transmural electrical stimulation with trains of 200-300 pulses produced contractions which were rapid in onset and recovery, and sometimes were biphasic. Contractions at both 5 Hz and 20 Hz were reduced by 50-70% after treatment with prazosin (0.1-1 microM). The remaining contractions were enhanced significantly by yohimbine (1 microM), were reduced very slightly by dihydroergotamine, and were largely abolished by guanethidine (1 microM). alpha,beta,m-ATP (1-100 microM) alone often enhanced neurogenic contractions (by 100-200%), whereas suramin (30 microM) alone reduced contractions by 48%.(ABSTRACT TRUNCATED AT 250 WORDS)
Morris
J L
JL
Department of Anatomy & Histology, School of Medicine, Flinders University of South Australia, Adelaide.
D000255:Adenosine Triphosphate / Q000037:antagonists & inhibitors / Q000494:pharmacology / Q000502:physiology*; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001158:Arteries / Q000502:physiology; D004423:Ear / Q000098:blood supply*; D004558:Electric Stimulation; D005260:Female; D006168:Guinea Pigs; D008297:Male; D009638:Norepinephrine / Q000037:antagonists & inhibitors / Q000494:pharmacology / Q000502:physiology*; D058914:Purinergic Antagonists; D013564:Sympathetic Nervous System / Q000502:physiology*; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*
D000319:Adrenergic beta-Antagonists; D058914:Purinergic Antagonists; D000255:Adenosine Triphosphate; D009638:Norepinephrine