Gardiner D S, Jackson R, Lindop G B
University Department of Pathology, Western Infirmary, Glasgow, UK.
Virchows Arch A Pathol Anat Histopathol. 1992;420(6):533-7. doi: 10.1007/BF01600259.
The glomerular peripolar cell may be a secretory component of the juxtaglomerular apparatus. To investigate this hypothesis we studied kidneys with the renin-angiotensin system activated by two different stimuli in order to compare the responses of peripolar cells and renin-secreting cells. We examined 10 human kidneys, removed for renal artery stenosis and 11 autopsy cases of Addison's disease with appropriate controls. We counted granulated peripolar cells in serial paraffin-embedded sections and renin-containing cells were quantified using an immunoperoxidase technique with an antiserum to human renin. There was a five-fold increase in the number of renin-containing cells in both renal artery stenosis and in untreated, but not in treated, Addison's disease. Peripolar cells were increased in number in three cases of renal artery stenosis, but were unaltered in both treated and untreated Addison's disease. Therefore, neither a reduction in renal perfusion pressure (renal artery stenosis), nor sodium depletion (Addison's disease) consistently affect peripolar cells in humans. These findings do not support the hypothesis that the peripolar cell is part of the juxtaglomerular apparatus.
肾小球极周细胞可能是球旁器的一个分泌成分。为了验证这一假说，我们研究了通过两种不同刺激激活肾素 - 血管紧张素系统的肾脏，以便比较极周细胞和肾素分泌细胞的反应。我们检查了10个因肾动脉狭窄而切除的人肾以及11例艾迪生病尸检病例，并设置了适当的对照。我们在连续石蜡包埋切片中计数颗粒状极周细胞，并使用抗人肾素抗血清的免疫过氧化物酶技术对含肾素细胞进行定量。在肾动脉狭窄组以及未经治疗而非经治疗的艾迪生病组中，含肾素细胞数量增加了五倍。在3例肾动脉狭窄病例中极周细胞数量增加，但在经治疗和未经治疗的艾迪生病组中极周细胞数量均未改变。因此，无论是肾灌注压降低（肾动脉狭窄）还是钠耗竭（艾迪生病），在人类中均未持续影响极周细胞。这些发现不支持极周细胞是球旁器一部分的假说。
