Electrophysiological analysis of the nature of adrenoceptors in the rat basilar artery during development

Abstract

1 The nature of adrenoceptors in basilar arteries of neonatal rats was investigated by means of electrophysiological techniques. 2 In immature (2–6 day postnatal) rats, micro-injection of noradrenaline elicited a depolarization which consisted of two components. The initial ‘fast’ component (time to peak of 0.3–4 s) was slightly reduced by phentolamine and was not antagonized by propranolol. The second ‘slow’ component (time to peak of about 50 s) was not blocked by phentolamine but was antagonized by low concentrations (10⁻⁷ M) of propranolol. 3 In immature rats, micro-injection of isoprenaline was more potent than noradrenaline in evoking the ‘slow’ depolarization but less effective in eliciting the ‘fast’ response. The pharmacology with respect to adrenoceptor antagonists of both components of the isoprenaline- and noradrenaline-induced depolarizations was similar. There was some evidence of inhibitory β-adrenoceptors in immature rat basilar vessels. 4 In adult rats (6 week old) noradrenaline produced a large ‘fast’ depolarization which was followed by a ‘slow’ tail response. Both components were not antagonized by phentolamine or propranolol. 5 It appears that in the basilar artery of neonatal rats there are excitatory α- and inhibitory β-adrenoceptors but the major responses to noradrenaline and isoprenaline are mediated by γ- and excitatory β-receptors. In adult animals the γ-adrenoceptor predominates. 6 Experiments were carried out in which agonists were applied by ionophoresis. These results confirm the presence of excitatory β-receptors in neonatal basilar vessels and show the response has slow kinetics and it is likely that the β-receptors are distributed uniformly over the smooth muscle surface. In adult animals it was not possible to elicit an excitatory β-receptor-mediated response. 7 The ionophoretic application of noradrenaline never evoked a perceptible depolarization which could be attributed to γ-adrenoceptor stimulation. This result is discussed in terms of receptor distribution with respect to synaptic function in a syncytium.