The effect of K deprivation on catecholamine (CA) secretion induced by transmural stimulation of the isolated perfused adrenal glands of the rat was studied. 2. In the absence of external K, secretion of CA evoked by transmural stimulation was greatly (2- to 7-fold) facilitated. The facilitation was inversely related to the frequency of stimulation. The duration of CA secretion upon stimulation was prolonged significantly in K-free medium as compared to that in Krebs solution. 3. CA secretion evoked by acetylcholine (ACh) in K-free Krebs solution was increased by about 40%, with little change in the duration of secretion. 4. Chronic denervation of the adrenal gland practically abolished secretory response induced by transmural stimulation without affecting secretion of CA by ACh. Perfusion of the denervated adrenal gland with K-free solution enhanced ACh-induced CA secretion by about 40%, and a secretory response to transmural stimulation became evident. 5. Spontaneous secretion of CA was increased from a control value of about 2 ng/min to 56 ng/min 35 min after perfusion with K-free Krebs solution. During enhanced spontaneous secretion, electrical stimulation of the adrenal gland produced facilitation of secretion. 6. Spontaneous secretion of CA in K-free medium was only slightly reduced by lowering Ca to 0.25 mM, but that evoked by stimulation was markedly depressed. However, spontaneous and evoked secretion in K-free medium were totally blocked upon removal of Ca and addition of 5 mM-EGTA. 7. Re-introduction of 2.5 mM-Ca 6 min after stimulation of the adrenal gland in 0.25 mM-Ca, K-free solution produced a marked secretory response. 8. Lowering of Ca to 0.25 mM immediately after stimulation of the adrenal gland in K-free solution significantly reduced the amounts of CA secreted in the post-stimulation period. 9. Ouabain (0.14-1.4 mM) did not enhance secretion of CA in unstimulated preparations or after transmural stimulation of the rat adrenal gland. ACh-induced secretion was more than doubled by ouabain. 10. Not only was spontaneous secretion of CA from the guinea-pig adrenal gland enhanced by K deprivation or ouabain, but secretion evoked by transmural stimulation or by ACh was also facilitated in K-free medium by ouabain (0.7-7.0 microM). 11. Enhanced secretion of CA in unstimulated preparations or after transmural stimulation of the adrenal gland, in the absence of K, has been attributed to the excess release of ACh from splanchnic nerve terminals. The enhanced release of ACh has been attributed to the elevation of free cellular CA resulting from blockade of the Na pump. On the other hand, ouabain facilitates CA secretin in the rat and guinea-pig adrenal glands predominantly by its effect on the chromaffin cells.
摘要
研究了钾缺乏对大鼠离体灌注肾上腺经壁刺激诱导的儿茶酚胺（CA）分泌的影响。2. 在无外源钾的情况下，经壁刺激诱发的CA分泌得到极大促进（2至7倍）。这种促进作用与刺激频率呈负相关。与在 Krebs 溶液中相比，在无钾培养基中刺激时 CA 分泌的持续时间显著延长。3. 在无钾的 Krebs 溶液中，乙酰胆碱（ACh）诱发的 CA 分泌增加约40%，分泌持续时间变化不大。4. 肾上腺慢性去神经支配实际上消除了经壁刺激诱导的分泌反应，而不影响 ACh 诱导的 CA 分泌。用无钾溶液灌注去神经支配的肾上腺可使 ACh 诱导的 CA 分泌增加约40%，并且对经壁刺激的分泌反应变得明显。5. 用无钾的 Krebs 溶液灌注35分钟后，CA的自发分泌从约2纳克/分钟的对照值增加到56纳克/分钟。在自发分泌增强期间，对肾上腺的电刺激产生分泌促进作用。6. 在无钾培养基中，将钙降至0.25毫摩尔/升时，CA的自发分泌仅略有减少，但刺激诱发的分泌则明显受到抑制。然而，在无钾培养基中，去除钙并添加5毫摩尔/升乙二醇双（2-氨基乙基醚）四乙酸（EGTA）后，自发和诱发分泌完全被阻断。7. 在0.25毫摩尔/升钙、无钾溶液中刺激肾上腺6分钟后重新引入2.5毫摩尔/升钙，产生明显的分泌反应。8. 在无钾溶液中刺激肾上腺后立即将钙降至0.25毫摩尔/升，显著减少刺激后时期分泌的CA量。9. 哇巴因（0.14至1.4毫摩尔/升）在未刺激的制剂中或大鼠肾上腺经壁刺激后不增强CA分泌。哇巴因使ACh诱导的分泌增加一倍以上。10. 不仅豚鼠肾上腺CA的自发分泌因钾缺乏或哇巴因而增强，而且在无钾培养基中，哇巴因（0.7至7.0微摩尔/升）也促进经壁刺激或ACh诱发的分泌。11. 在无钾的情况下，未刺激的制剂中或肾上腺经壁刺激后CA分泌增强归因于内脏神经末梢ACh释放过多。ACh释放增加归因于钠泵阻断导致细胞内游离CA升高。另一方面，哇巴因主要通过其对嗜铬细胞的作用促进大鼠和豚鼠肾上腺的CA分泌。
