Developmental disappearance of excitatory α₁ adrenoceptor function in the oesophagus of chick embryo

Abstract

1 Developmental change in the response to noradrenaline (NA) and 5-hydroxytryptamine (5-HT) was investigated in the chick oesophagus between 9 and 21 days of incubation and 4 days after hatching.2 NA (5pM) produced a significant contraction in the oesophagus at 9 days of incubation. The NA-induced contraction progressively decreased with development and changed to an inhibition of spontaneous contraction or a small relaxation by 17 days of incubation. 3 The NA-induced contractile response was inhibited by phentolamine (2.7 pM) and prazosin (0.55pM). Phenylephrine (5pM) but not clonidine (5-50pM), also induced a contraction at early stages. The relaxation response to NA was sensitive to the fl-receptor blocker, carteolol (3.4 pM). 4 Pretreatment with carteolol unmasked the contractile responses to NA in preparations at 17-19 days of incubation. However, even in the presence of carteolol, the contraction produced by NA decreased and disappeared by the time of hatching. This change in response to NA is accompanied by a decline in the pD2 value. The response to phenylephrine (5pM) followed the same pattern as that to NA. 5The maximum binding sites of [3H]-dihydroergocryptine to the crude membrane preparation from oesophagus changed little at 13, 17 and 21 days of incubation. 6 Isoprenaline (Iso, 0.01-20 pM) caused a carteolol-sensitive relaxation in the carbachol-contracted oesophagus after 13 days of incubation. The sensitivity (pD2 value) to Iso decreased slightly up to 17 days of incubation.7 5-HT (10pM) caused a contraction in the oesophagus after 13 days of incubation and the amplitude of the response increased up to 17 days of incubation. The response to 5-HT was abolished by methysergide (1 pM) but not by tetrodotoxin (0.78 pM) or atropine (1 pM) at every stage tested. 8 These results suggest that the response to NA changed from an ax-adrenoceptor-mediated contraction to a #-receptor-mediated relaxation during the embryonic period, resulting partly from the decline and disappearance of excitatory xP-receptor function in the chick oesophagus.