Presynaptic dopamine DA2-receptors in rabbit jejunal arteries. An electrophysiological study.
Excitatory junction potentials (e.j.ps) evoked by nerve stimulation with 15 pulses at 1 Hz were recorded from muscle cells of rabbit isolated jejunal arteries. LY 171555 1 mumol/l, SKF 38393 10 mumol/l, dopamine 10 mumol/l and clonidine 0.1 mumol/l depressed all e.j.ps in the train. The percentage inhibition was inversely related to the number of pulses. S- and R-sulpiride, 10 mumol/l, domperidone 1 mumol/l, SCH 23390 1 mumol/l and rauwolscine 1 mumol/l did not change, or even depressed the first e.j.ps. Of these compounds only S- and R-sulpiride, 10 mumol/l and rauwolscine 1 mumol/l facilitated the late e.j.ps. The percentage facilitation increased with the number of pulses until a maximum was reached; rauwolscine 1 mumol/l had the largest effect. S- and R-sulpiride, 10 mumol/l, as well as domperidone 1 mumol/l antagonized the action of LY 171555 1 mumol/l. S-Sulpiride was more potent than its R-isomer. SCH 23390 1 mumol/l and rauwolscine 1 mumol/l blunted the effect of SKF 38393 10 mumol/l. Rauwolscine 1 mumol/l slightly reduced the inhibition by dopamine 10 mumol/l; S-sulpiride 10 mumol/l was antagonistic only in the presence of rauwolscine 1 mumol/l. When rauwolscine 1 mumol/l, prazosin 0.1 mumol/l, propranolol 1 mumol/l and cocaine 10 mumol/l was added to the medium, dopamine 10 mumol/l continued to produce the same depression of e.j.ps, as in the absence of these compounds. Under such conditions S-sulpiride 10 mumol/l also counteracted dopamine 10 mumol/l. Rauwolscine 1 mumol/l prevented the effect of clonidine 0.1 mumol/l. The antagonists were not absolutely selective against only one type of agonist. We suggest that both presynaptic DA2- and postsynaptic DA1-receptors are present in rabbit jejunal arteries. The activation of either receptor-type may depress the e.j.ps. Dopamine interferes with neuroeffector transmission due to alpha 2-adrenoceptor agonist properties; its DA2-effect is unmasked only after alpha 2-adrenoceptor blockade. There was no evidence for a co-transmitter function of dopamine.
Nörenberg
W
W
Department of Pharmacology, University of Freiburg, Federal Republic of Germany.
Illes
P
P
D015647:2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine / Q000494:pharmacology; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000818:Animals; D001552:Benzazepines / Q000494:pharmacology; D004294:Domperidone / Q000494:pharmacology; D004347:Drug Interactions; D004558:Electric Stimulation; D004594:Electrophysiology; D004873:Ergolines / Q000494:pharmacology; D005260:Female; D066298:In Vitro Techniques; D007583:Jejunum / Q000098:blood supply; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D019257:Quinpirole; D011817:Rabbits; D011954:Receptors, Dopamine / Q000187:drug effects*; D012039:Regional Blood Flow / Q000187:drug effects; D013469:Sulpiride / Q000494:pharmacology; D013569:Synapses / Q000187:drug effects; D015016:Yohimbine / Q000494:pharmacology
D000316:Adrenergic alpha-Agonists; D001552:Benzazepines; D004873:Ergolines; D011954:Receptors, Dopamine; D019257:Quinpirole; D015016:Yohimbine; D004294:Domperidone; D015647:2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine; D013469:Sulpiride