Extracellular calcium and cholinergic stimulation of isolated canine parietal cells.
Extracellular calcium and cholinergic stimulation of isolated canine parietal cells.
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分离的犬壁细胞的细胞外钙和胆碱能刺激。
DOI：
10.1172/jci110243
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发表时间：
1981
期刊：
影响因子：
--
通讯作者：
Soll,AH
中科院分区：
文献类型：
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作者：
Soll,AH
用胶原酶和EDTA处理犬胃底粘膜分离的细胞，并通过淘析器转子中的速度分离富集，研究了钙门控在胆碱能刺激壁细胞功能中的作用。监测积累的[14 C]氨基比林作为壁细胞反应的指标，刺激卡巴胆碱，但不是组胺，是高度依赖于细胞外钙的浓度。将壁细胞培养在0-.1 mM钙中，而不是通常的1.8 mM浓度，使对100 μ M卡巴胆碱的反应降低92 +/-2%，而组胺刺激受损28 +/-5%。细胞外钙的类似减少抑制了对胃泌素（100 nM）的反应67 +/-7%。在低细胞外钙浓度下发现的胆碱能刺激的损伤随着钙的再加入而迅速逆转。镧可阻断钙跨膜移动，对氨基比林蓄积的促分泌素刺激产生类似的作用模式，100 μ M镧抑制卡巴胆碱刺激83 +/-2%。该浓度的镧抑制了40 +/- 7%的胃泌素刺激，仅抑制了12 +/-9%的组胺刺激。卡巴胆碱，而不是组胺或胃泌素，刺激45 Ca ++摄取。卡巴胆碱刺激的钙吸收量与所检查组分的壁细胞含量相关（r = 0.88），并且在卡巴胆碱浓度从1 μ M到1 mM的范围内是剂量响应性的。阿托品（100 nM）引起可克服的抑制，氨甲酰胆碱和阿托品对钙摄取的影响与它们对氧消耗的影响相关（r = 0.93）和[14 C]-氨基比林蓄积（r = 0.90）。细胞预装45 Ca ++失去细胞钙在一个时间依赖性的方式，然而，这种速度的出口没有加速治疗组胺，胃泌素，或卡巴胆碱，因此未能牵连动员细胞内钙激活壁细胞功能的主要机制。这些数据表明胆碱能药物刺激壁细胞功能和增强钙内流之间存在密切联系。
The role of calcium gating in cholinergic stimulation of the function of parietal cells was studied using cells isolated from canine fundic mucosa by treatment with collagenase and EDTA and enriched by velocity separation in an elutriator rotor. Monitoring the accumulation of [14C[ aminopyrine as an index of parietal cell response, stimulation by carbachol, but not by histamine, was highly dependent upon the concentration of extracellular calcium. Incubation of parietal cells in 0-.1 mM calcium, rather than the usual 1.8 mM concentration, reduced the response to 100 microM carbachol by 92 +/- 2%, whereas histamine stimulation was impaired by 28 +/- 5%. A similar reduction in extracellular calcium suppressed the response to gastrin (100 nM) by 67 +/- 7%. The impairment of cholinergic stimulation found at low extracellular calcium concentrations was rapidly reversed with the readdition of calcium. Lanthanum, which blocks calcium movement across membranes, caused a similar pattern of effects on secretagogue stimulation of aminopyrine accumulation, with 100 microM lanthanum suppressing carbachol stimulation by 83 +/- 2%. This concentration of lanthanum suppressed gastrin stimulation by 40 +/- 7% and histamine stimulation by only 12 +/- 9%. Carbachol, but not histamine nor gastrin, stimulated 45Ca++ uptake. The magnitude of carbachol-stimulated calcium uptake correlated with the parietal cell content of the fractions examined (r = 0.88), and was dose responsive over carbachol concentrations from 1 microM to 1 mM. Atropine (100 nM) caused surmountable inhibition, and these effects of carbachol and atropine on calcium uptake correlated with their effects on oxygen consumption (r = 0.93) and [14C]-aminopyrine accumulation (r = 0.90). Cells preloaded with 45Ca++ lost cellular calcium in a time-dependent fashion; however, this rate of egress was not accelerated by treatment with histamine, gastrin, or carbachol, thus failing to implicate mobilization of intracellular calcium as primary mechanism for activation of parietal cell function. These data indicate a close link between stimulation of parietal cell function and enhancement of calcium influx by cholinergic agents.