SUMMARY1. Simultaneous studies on the secretary response of amylase and the neurotransmitter receptors ofrat parotid gland, after brieftreatment with agonists, showed selective alteration in /1-adrenoceptors with specific change in amylase secretion, suggesting a regulatory role of the receptors in the secretary response.2. The fl-adrenergic agonist (± )-isoprenaline (IPR) stimulated amylase secretion from rat parotid tissues much more than did the same concentration ofan a-adrenergic or cholinergic agonist.3. The stimulatory effects of JPR were studied by pre-treating rat parotid tissues with IPR for 10 min and then incubating the tissue in fresh medium for 10 min.Pre-treatment with 10 ,pM-IPR for 10 min resulted in increased amylase secretion during further incubation with IPR and also in a lower EC60 value of amylase secretion for IPR.4. This treatment also resulted in selective changes in the number and affinity of 8. The alteration in fl-adrenoceptors was parallel with a change in amylase secretion after IPR pre-treatment, but not with a change in cyclic AMP content.

Abstract-Radiolabeled E-643, a newly developed antihypertensive compound, bound specifically to a preparation obtained from rat brain with a maximum of 85 f moles of binding sites per mg protein and a dis sociation constant of 0.59 nM. Prazosin markedly inhibited the binding, while yohimbine and clonidine were only weak inhibitors.Other character istics of the binding of [3H] E-643 to the brain and its specific binding to preparations of peripheral rat organs were also studied. The present findings suggest that [3H]E-643 is useful for labeling a,-adrenoceptors.

1 The effect of dopamine on amylase secretion by rat parotid tissue was examined in vitro.2 Dopamine induced marked amylase secretion from the tissue in a dose-dependent manner. Its EC50 value was about 4 gM and the maximal response was obtained at a concentration of 100 AM.3 The dopamine-induced secretion was inhibited by the dopamine-antagonists haloperidol, (+)-butaclamol and spiroperidol. 4 Atropine reduced the dopamine-induced secretion significantly, and physostigmine enhanced the secretion. 5 Parasympathectomy of the gland resulted in a significant decrease in the dopamine-induced secretion, but did not reduce the secretion induced by dopamine with atropine. 6 Dopamine-induced ACh release from parasympathetic nerve terminals in the tissue was studied in tissue preparations that had been loaded with [3H]-choline. Dopamine elicited Ca2+-sensitive tritium release, and dopamine antagonists or parasympathectomy prevented this release. 7 Sympathectomy or reserpine treatment of rats resulted in significant decrease in the dopamineinduced secretion, but increase in noradrenaline (NA)-or isoprenaline-induced secretion. 8 Dopamine-induced NA release was studied by preloading the parotid tissue with [3H]-NA. Dopamine induced Ca2"-sensitive tritium release, and dopamine antagonists or sympathectomy prevented the release. 9 Several lines of circumstantial evidence strongly suggested that dopamine has a specific site for action in the parotid tissue that is independent of NA receptors. 10 In sympathectomized or reserpine-treated glands, atropine completely inhibited the dopamineinduced amylase secretion, suggesting that dopamine did not have a direct effect on postsynapses. 11 These findings indicate that dopamine induces amylase secretion in two indirect ways mediated through ACh and NA released from parasympathetic and sympathetic nerve terminals, respectively.

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Abstract-The stimulatory effect