Hata F, Ishida H, Kagawa K, Kondo E, Kondo S, Noguchi Y
J Physiol. 1983 Aug;341:185-96. doi: 10.1113/jphysiol.1983.sp014800.
Simultaneous studies on the secretory response of amylase and the neurotransmitter receptors of rat parotid gland, after brief treatment with agonists, showed selective alteration in beta-adrenoceptors with specific change in amylase secretion, suggesting a regulatory role of the receptors in the secretory response. The beta-adrenergic agonist (+/-)-isoprenaline (IPR) stimulated amylase secretion from rat parotid tissues much more than did the same concentration of an alpha-adrenergic or cholinergic agonist. The stimulatory effects of IPR 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 microM-IPR for 10 min resulted in increased amylase secretion during further incubation with IPR and also in a lower EC50 value of amylase secretion for IPR. This treatment also resulted in selective changes in the number and affinity of beta-adrenoceptors, assessed by measuring binding of [3H]dihydroalprenolol (DHA): the maximal binding sites increased from 286/357 f-mole to mg protein and the IC50 value (the concentration for 50% inhibition of specific [3H]DHA binding) of beta-agonists, not antagonists, decreased significantly. An increase in the period of pre-treatment with IPR to 30 min resulted in a decrease in the maximal binding sites of beta-adrenoceptors and a decrease in amylase secretion during further incubation with IPR. Experiments with other agonists showed that supersensitivity of the secretory response was induced specifically by beta-agonists. Binding studies with [3H]WB-4101 and [3H]quinuclidinyl benzilate showed that alpha-adrenoceptors and muscarinic ACh receptors in rat parotid did not change under the conditions tested. The alteration in beta-adrenoceptors was parallel with a change in amylase secretion after IPR pre-treatment, but not with a change in cyclic AMP content.
在用激动剂进行短暂处理后，对大鼠腮腺淀粉酶分泌反应和神经递质受体进行的同步研究表明，β-肾上腺素能受体发生选择性改变，同时淀粉酶分泌也有特定变化，这表明这些受体在分泌反应中具有调节作用。β-肾上腺素能激动剂（±）-异丙肾上腺素（IPR）刺激大鼠腮腺组织分泌淀粉酶的作用，比相同浓度的α-肾上腺素能或胆碱能激动剂要强得多。通过用IPR预处理大鼠腮腺组织10分钟，然后将组织在新鲜培养基中孵育10分钟，研究了IPR的刺激作用。用10μM-IPR预处理10分钟，在进一步与IPR孵育期间导致淀粉酶分泌增加，并且IPR刺激淀粉酶分泌的半数有效浓度（EC50）值降低。该处理还导致通过测量[3H]二氢阿普洛尔（DHA）结合来评估的β-肾上腺素能受体数量和亲和力的选择性变化：最大结合位点从286/357 f-摩尔/毫克蛋白增加，β-激动剂而非拮抗剂的半数抑制浓度（IC50）值（抑制特异性[3H]DHA结合50%的浓度）显著降低。将IPR预处理时间延长至30分钟，导致β-肾上腺素能受体的最大结合位点减少，并且在进一步与IPR孵育期间淀粉酶分泌减少。用其他激动剂进行的实验表明，分泌反应的超敏性是由β-激动剂特异性诱导的。用[3H]WB-4101和[3H]喹核醇基苯甲酸酯进行的结合研究表明，在所测试的条件下，大鼠腮腺中的α-肾上腺素能受体和毒蕈碱型乙酰胆碱受体没有变化。IPR预处理后β-肾上腺素能受体的改变与淀粉酶分泌的变化平行，但与环磷酸腺苷含量的变化无关。
