UREA TRANSPORT AND THE URINARY CONCENTRATING MECHANISM

尿素运输和尿液浓缩机制

• 批准号: 3966566
• 负责人: M A KNEPPER
• 金额: --
• 依托单位: NATIONAL HEART, LUNG, AND BLOOD INSTITUTE
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/3966566
• 关键词: active transport; arginine vasopressin; biological fluid transport; body fluid osmolarity; colorimetry; diuresis; epithelium; ion transport; kidney metabolism; mathematical model; membrane permeability; model design /development; radiotracer; renal medulla; renal tubular transport; tissue /cell culture; urea

The papillary surface epithelium has been proposed to play an important role in the urinary concentrating mechanism. We undertook studies to determine what transporters are present in this epithelium. The papillary surface epithelium was dissected from the surface of the rabbit renal papilla and mounted in a perfusion chamber which allowed both sides to be perfused independently. Cell volume was measured at 25 degrees C using computerized quantitative microscopy which allows continuous measurement of cell volume of the living tissue. Addition of ouabain (0.1 mM) to the basolateral side of the epithelium induced a 20% volume increase. This volume increase was completely inhibited by removal of apical bath NaCl, sodium, chloride, or potassium, but not by removal of urea. As little as 1 nanomolar bumetanide in the apical bath completely inhibited the ouabain-induced cell swelling. Changes in apical osmolality resulting from the addition or removal of NaCl caused cell volume changes that were greater than could be accounted for by osmotic water flow alone. This hyper-response was blocked by bumetanide and was stimulated by vasopressin. These observations are consistent with the presence of Na-K-ATPase on the basolateral membrane and a bumetanide-sensitive, vasopressin-responsive Na-K-Cl cotransporter in the apical membrane. These results are consistent with transpithelial transport of sodium chloride by this epithelium which could modify the composition of the pelvic urine.

乳头状表面上皮细胞被认为在 在尿液浓缩机制中的作用。 我们进行了研究， 确定上皮细胞中有哪些转运蛋白 乳头 从兔肾表面解剖表面上皮 乳头和安装在灌注室，允许双方都是 独立灌注。 细胞体积在25 ° C下测量，使用 计算机定量显微镜，允许连续测量 活组织的细胞体积。 将哇巴因（0.1 mM）添加至 上皮的基底外侧诱导了20%的体积增加。 这 体积增加完全被去除顶端浴NaCl抑制， 钠、氯化物或钾，但不是通过除去尿素。 少至1 纳摩尔布美他尼在根尖浴完全抑制 哇巴因诱导的细胞肿胀。 顶端渗透压摩尔浓度的变化 加入或去除NaCl引起细胞体积的变化， 比渗透水单独流动所能解释的要大。 这 超反应被布美他尼阻断， 加压素 这些观察结果与存在的 基底外侧膜上的Na-K-ATP酶和布美他尼敏感， 顶膜中的加压素反应性Na-K-Cl协同转运蛋白。 这些 结果与氯化钠的透皮转运一致， 这种上皮可以改变盆腔尿液的成分。