Martinez J R, Quissell D O, Giles M
J Pharmacol Exp Ther. 1976 Aug;198(2):385-94.
Slices of submaxillary gland were incubated in vitro in an enriched Krebs-Ringer-bicarbonate medium gassed with 95% O2-5% CO2 at 37 degrees C and the release of K+ into the medium was monitored after stimulation with alpha and beta adrenergic secretagogues under a variety of experimental conditions. K+ was released by the slice system after addition of norepinephrine, epinephrine or phenylephrine, but not after addition of isoproterenol. The extent of K+ release after norepinephrine depends on the dose of secretagogue and is higher when glucose, adenine and inosine, or all three substrates are absent from the medium. The effect of norepinephrine on K+ release is reversed by phentolamine but not by propranolol. Phentolamine also causes a 9.4-fold shift to the right in the dose-response curve to norepinephrine. Addition of ouabain to the incubation medium results in a higher extent of K+ release and prevents the reversal caused by phentolamine. The response to norepinephrine fails to occur when Ca++ is absent from the medium, either by chelation with ethylene glycol bis (beta-amino-ethyl ether)-N,N'-tetraacetic acid or by elimination from the Krebs-Ringer solution, and shows gradations depending on the Ca++ content of the medium. By itself, however, Ca++ does not induce K+ release from the slice system. The following conclusions are derived from these observations: 1) the release of K+ ions from the submaxillary gland is mediated by alpha adrenergic receptors; 2) the net amount of K+ released is the result of two opposing and almost simultaneous mechanisms, a passive extrusion and an active reuptake; 3) the active reuptake of K+ depends on the availability of energy and is mediated through the ouabain-sensitive Na+-K+ activated adenosine triphosphatase; 4) the reaction is critically dependent on the presence of Ca++ in the incubation medium and probably involves an influx of Ca++ upon stimulation with alpha adrenergic secretagogues.
将颌下腺切片置于富含 Krebs - Ringer - 碳酸氢盐的培养基中,于 37℃用 95% O₂ - 5% CO₂ 进行体外孵育,并在多种实验条件下,用 α 和 β 肾上腺素能促分泌剂刺激后,监测钾离子(K⁺)释放到培养基中的情况。加入去甲肾上腺素、肾上腺素或苯肾上腺素后,切片系统会释放 K⁺,但加入异丙肾上腺素后则不会。去甲肾上腺素作用后 K⁺ 的释放程度取决于促分泌剂的剂量,当培养基中不存在葡萄糖、腺嘌呤和肌苷或这三种底物都不存在时,释放程度更高。酚妥拉明可逆转去甲肾上腺素对 K⁺ 释放的作用,而普萘洛尔则不能。酚妥拉明还会使去甲肾上腺素的剂量 - 反应曲线向右移动 9.4 倍。向孵育培养基中加入哇巴因会导致 K⁺ 释放程度更高,并阻止酚妥拉明引起的逆转。当培养基中通过与乙二醇双(β - 氨基乙醚)- N,N'- 四乙酸螯合或从 Krebs - Ringer 溶液中去除而不存在钙离子(Ca²⁺)时,对去甲肾上腺素的反应不会发生,且反应程度取决于培养基中 Ca²⁺ 的含量。然而,单独的 Ca²⁺ 本身并不会诱导切片系统释放 K⁺。从这些观察结果得出以下结论:1)颌下腺中 K⁺ 离子的释放由 α 肾上腺素能受体介导;2)释放的 K⁺ 净量是两种相反且几乎同时发生的机制的结果,一种是被动外排,另一种是主动再摄取;3)K⁺ 的主动再摄取取决于能量的可用性,并通过对哇巴因敏感的 Na⁺ - K⁺ 激活的三磷酸腺苷酶介导;4)该反应严重依赖于孵育培养基中 Ca²⁺ 的存在,并且可能涉及在用 α 肾上腺素能促分泌剂刺激时 Ca²⁺ 的内流。