Engström K G, Sävendahl L
Department of Histology and Cell Biology, University of Umeå, Sweden.
Cytometry. 1995 May 1;20(1):7-13. doi: 10.1002/cyto.990200103.
The size and shape of growth hormone (GH)-producing rat type-II somatotrophs was studied during osmotic manipulation. When somatotrophs were exposed to large osmotic stress (200 and 225 mOsm), the peak projected cell area (PCA) was 132.9% +/- 12.6% and 116.8% +/- 2.8% (P < 0.01) and triggered a regulatory volume decrease (RVD) to avoid lysis. At lower osmotic stress (250 mOsm), the rate of swelling was slower, and the volume reached a steady state at 109.4% +/- 2.4% (P < 0.05) and was without RVD. At 275 and 287 mOsm, the swelling was delayed [PCA peak at 3-4 min; 105.8% +/- 1.5% (P < 0.05) and 104.2% +/- 1.7%] and then showed repeated synchronized cycles of swelling and shrink-age (P < 0.05). The data suggest that somatotrophs may have more than one mechanism for volume regulation. One mechanism is for large swelling (classic RVD response), whereas the other represents more physiological mechanisms for regulating the cell volume within a more limited geometry range. For low osmotic stress (250-287 mOsm), the somatotrophs became less spherical during swelling and, thus, were without membrane dilation. Therefore, this type of volume regulation must work independently from membrane stress. Related volume regulation mechanisms may underlie the previously observed volume fluctuations in somatotrophs seen during secretory stimulation with GH-releasing hormone.
在渗透操作过程中,对产生生长激素(GH)的大鼠II型生长激素细胞的大小和形状进行了研究。当生长激素细胞暴露于较大的渗透压应激(200和225毫渗量浓度)时,峰值投影细胞面积(PCA)分别为132.9%±12.6%和116.8%±2.8%(P<0.01),并引发调节性容积减小(RVD)以避免细胞裂解。在较低的渗透压应激(250毫渗量浓度)下,肿胀速率较慢,容积在109.4%±2.4%时达到稳定状态(P<0.05),且无RVD。在275和287毫渗量浓度时,肿胀延迟[PCA峰值出现在3 - 4分钟;105.8%±1.5%(P<0.05)和104.2%±1.7%],然后出现反复同步的肿胀和收缩循环(P<0.05)。数据表明,生长激素细胞可能有不止一种容积调节机制。一种机制用于应对较大肿胀(经典RVD反应),而另一种代表在更有限的几何范围内调节细胞容积的更多生理机制。对于低渗透压应激(250 - 287毫渗量浓度),生长激素细胞在肿胀过程中变得不那么呈球形,因此没有膜扩张。所以,这种类型的容积调节必须独立于膜应激起作用。相关的容积调节机制可能是先前观察到的在用生长激素释放激素进行分泌刺激时生长激素细胞中出现的容积波动的基础。