Regulation of beta-agonist-induced secretion of amylase from rat parotid acini by K^+-channels

结合β-肾上腺素受体功能研究了K^+通道在调节大鼠腮腺腺泡淀粉酶分泌中的作用。结果表明，增加细胞外K^+浓度或加入K^+通道阻断剂均能促进淀粉酶分泌。在几种K^+通道阻断剂中，四乙基铵、蜂毒肽和Charybdotoxin分别使淀粉酶分泌增加48%、69%和84%，低浓度去甲肾上腺素（10 μ <-7>M）可使分泌增加154%，与四乙基铵同时使用时产生协同效应，产生371%的刺激。四乙基铵与低浓度卡巴胆碱（10 μ M）联合使用时<-6>无协同效应。10 μ M去甲肾上腺素<-6>可使分泌增加313%，而10 μ <-3>M缬氨霉素（一种K^+离子载体）可使其减少116%。缬氨霉素对卡巴胆碱（10 μ <-5>M）诱导的分泌无影响。生长抑素（10 μ <-5>M）和吗啡（10 μ M）也可减少去甲肾上腺素诱导的淀粉酶分泌。这些结果提示Ca^2+<-4>-腮腺腺泡淀粉酶分泌过程中去甲肾上腺素激活的K^+通道。

The involvement of K^+ channels in regulating secretion of amylase from isolated rat parotid acini was studied in conjunction with beta-adrenoceptor function.It was observed that increasing the concentration of extracellular K^+ or adding K^+ channel blockers enhanced the secretion of amylase.Among several K^+ channel blockers, tetraethylammonium, apamin and charybdotoxin were effective to enhance secretion by 48, 69, and 84%, respectively.Glibenclamide was without effect.A low concentration of noradrenaline (10^<-7> M) enhanced secretion by 154% and its simultaneous application with tetraethylammonium gave a synergistic effect, producing 371% stimulation.Combination of tetraethylammonium and a low concentration of carbachol (10^<-6> M) did not give the synergistic effect.Noradrenaline at the concentration of 10^<-6> M enhanced secretion by 313% and this was reduced to 116% by 10^<-3> M valinomycin, a K^+ ionophore.Valinomycin was without effect on carbachol (10^<-5> M)-induced secretion.Somatostatin (10^<-5> M) and morphine (10^<-4> M) also reduced noradrenaline-induced scretion of aimylase.These results suggested the regulation of Ca^<2+> -activated K^+ channels by noradrenaline in amylase secretory processes in parotid acini.