CELLULAR CONTROL OF SALIVARY BUFFER CAPACITY

碳酸氢盐浓度(HCO减去)的主函数 唾液是用来缓冲口腔酸碱度变化的。HCOminus是 由唾液腺的腺泡细胞通过 受环核苷酸控制的氯通道和 胞质钙。因此，我得出结论，唾液缓冲能力 直接受次生信使浓度调节的部分 腺泡细胞的细胞质。在本应用程序中，我将展示 Phi和细胞质之间存在紧密的、相反的关系。 钙。工作假设是细胞质氢离子(即， Phi)在激活过程中抑制钙内流。这一假说预言 从腮腺细胞流出的HCOminus是一种自我限制 现象(即，涉及2个细胞质的负反馈调节 离子--钙和氢)。我的初步证据显示 胞质钙受phi的直接影响 两性关系。还有证据表明，Na+/Ca++交换和 表面膜的钙泵对pH敏感。如果这个 假说可以被证明，然后这将确定腺泡细胞如何 在不危及自身缓冲能力的情况下分泌HCO- 引起细胞活化的phi降低。也是这项研究 将给我们提供线索，S负责的机制的性质 在激活过程中钙的内流是一个主要的争议点。 此应用程序中的实验将：1)建立关系 Phi和胞质钙之间的精确、定量关系和2) 表征对pH敏感的钙离子转运体。这 信息对于为调查 控制腺泡细胞的负反馈调节的存在 生理学。

The principal function of the bicarbonate concentration (HCOminus) of saliva is to buffer changes in the pH of the oral cavity. HCOminus is secreted by the acinar cells of the salivary glands into the lumen through the chloride channel which is under the control of cyclic nucleotides and cytoplasmic calcium. Thus I conclude that salivary buffer capacity is in part directly regulated by the concentration of secondary messengers in the cytoplasm of acinar cells. In this application, I shall show that there is a tight, inverse relationship between pHi and cytoplasmic calcium. The working hypothesis is that cytoplasmic hydrogen ions (i.e., pHi) inhibit calcium influx during activation. This hypothesis predicts that the efflux HCOminus from the parotid cell is a self-limiting phenomenon (i.e., negative feedback regulation involving 2 cytoplasmic ions--calcium and hydrogen). My preliminary evidence shows that cytoplasmic calcium is influenced by pHi in a directly varying relationship. There is also evidence that the Na+/Ca++ exchange and calcium pump of the surface membrane is sensitive to pHi. If this hypothesis could be proven, then this would establish how acinar cells secreted HCOminus without jeopardizing their own capacity to buffer the decrease in pHi that occasions cellular activation. Also this research would give us clues s to the nature of the mechanism responsible for the influx of calcium during activation which is a point of major controversy. The experiments in this application will: 1) establish the relationship between pHi and cytoplasmic calcium in precise, quantitative terms and 2) characterize the pHi-sensitive transporters of calcium ions. This information is essential to establish a foundation for investigating the presence of negative-feedback regulation that controls acinar cell physiology.