pSecretory vesicles from pancreatic acinar cells have recently been shown to release Casup2+/sup after stimulation with Ins(1,4,5)iP/isubi/i3/sub [Gerasimenko, Gerasimenko, Belan and Petersen, (1996) Cell b84/b, 473-480]. These observations have been used in support of the hypothesis that Casup2+/sup release from secretory vesicles could be an important component of stimulus secretion coupling in exocrine acinar cells. In the rat, ligation of the parotid duct causes a reversible atrophy of the parotid gland. Most notably, after atrophy the acinar cells are reduced in size and no longer contain secretory vesicles [Liu, Smith, and Scott (1996) J. Dent. Res. b74/b, 900]. We have measured cytosolic free-Casup2+/sup concentration ([Casup2+/sup]subi/sub) in single, acutely isolated, rat parotid acinar cells, and compared Casup2+/sup mobilization in response to acetylcholine (ACh) stimulation in cells obtained from control animals to that in cells lacking secretory vesicles obtained after atrophy of the parotid gland. Application of 50-5000 nM ACh to control cells gave rise to a typical, dose-dependent, biphasic increase in [Casup2+/sup]subi/sub, of which the later, plateau, phase was acutely dependent on the extracellular Casup2+/sup concentration. An identical pattern of response was observed with cells obtained from atrophic glands. Low concentrations of ACh (10-100 nM) occasionally produced [Casup2+/sup]subi/sub oscillations of a similar pattern in cells from both control and atrophic glands. We were able to show that Casup2+/sup rises first in the apical pole of the cell and the increase then spreads to the rest of the cell in cells from control glands but not in cells from atrophic glands. However, at present we are unable to determine whether this is due to the lack of secretory vesicles or whether the separation is too small to measure in the smaller acinar cells obtained from atrophic glands. We conclude therefore, that secretory vesicles make no significant contribution to overall Casup2+/sup mobilization in rat parotid acinar cells, nor are they required for oscillatory changes in [Casup2+/sup]subi/sub to occur. However we are unable to eliminate completely any role for secretory vesicles in initiating Casup2+/sup mobilization at the apical pole of the cell./p
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机译：>最近发现胰腺腺泡细胞分泌的囊泡在用Ins（1,4,5） P 刺激后释放Ca 2 + 3 [Gerasimenko，Gerasimenko，Belan and Petersen，（1996）Cell 84 ，473-480]。这些观察结果被用于支持从分泌小泡释放Ca 2 + 可能是外分泌腺泡细胞中刺激分泌耦合的重要组成部分这一假说的证据。在大鼠中，腮腺导管的结扎可导致腮腺的可逆萎缩。最明显的是，萎缩后，腺泡细胞的大小减小，不再包含分泌性囊泡[Liu，Smith，和Scott（1996）J.Dent。 Res。 74 ，900]。我们测量了单个急性分离的大鼠腮腺腺泡细胞中胞质游离Ca 2 + 的浓度（[Ca 2 + ] i ），并比较了从对照动物获得的细胞中乙酰胆碱（ACh）刺激对Ca 2 + 的动员与腮腺萎缩后缺乏分泌性囊泡的细胞的动员。将50-5000 nM ACh应用于对照细胞会导致[Ca 2 + ] i 呈典型的剂量依赖性双相增加，其中后期，阶段严重依赖于细胞外Ca 2 + 浓度。从萎缩性腺获得的细胞观察到相同的反应模式。低浓度的ACh（10-100 nM）有时会在对照和萎缩性腺细胞中产生类似模式的[Ca 2 + ] i 振荡。我们能够证明，Ca 2 + 首先在细胞的顶端生长，然后在控制腺的细胞中扩散，然后扩散到其余的细胞，而在萎缩性腺细胞中则没有扩散。然而，目前我们无法确定这是由于缺乏分泌性囊泡还是由于分离作用太小而无法在萎缩性腺体获得的较小腺泡细胞中进行测量。因此，我们得出结论，分泌性囊泡对大鼠腮腺腺泡细胞中的整体Ca 2 + 动员没有显着贡献，也不是[Ca 2 + ]振荡变化所必需的。 i 发生。然而，我们无法完全消除分泌小泡在细胞顶极启动Ca 2 + 动员的任何作用。
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