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

研究了K^+通道在调节离体大鼠腮腺腺腺淀粉酶分泌中的作用，并结合β -肾上腺素能受体的功能。增加细胞外K^+浓度或添加K^+通道阻滞剂可促进淀粉酶的分泌。在几种K^+通道阻滞剂中，四乙基铵、apamin和charybdotoxin的促分泌效果分别为48%、69%和84%。格列本脲无效。低浓度的去甲肾上腺素（10^<-7> M）可使分泌增强154%，与四乙基铵同时应用可产生协同效应，产生371%的刺激。四乙基铵与低浓度（10^<-6> M）的组合没有产生协同效应。当去甲肾上腺素浓度为10^<-6> M时，可使分泌量增加313%，而当K^+离子载体valinomycin浓度为10^<-3> M时，可使分泌量减少116%。Valinomycin对carbachol （10^<-5> M）诱导的分泌无影响。生长抑素（10^<-5> M）和吗啡（10^<-4> M）也能降低去甲肾上腺素诱导的淀淀酶分泌。提示去甲肾上腺素对腮腺腺淀粉酶分泌过程中Ca^<2+>激活的K^+通道的调节作用。

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.