Cellular Mechanisms and Regulation of Intestinal Potassium Transport

钾是人体中含量最丰富的阳离子之一，具有多种生理功能。本研究旨在阐明肠道K^+转运的细胞机制和调控。结果表明：；(1)在人体研究中，摄入钾或注射钾后尿钾排泄伴随着血液K^+升高；(2)在大鼠研究中，以聚乙二醇作为不可吸收的标志物，摄入的K^+主要在空肠近端吸收，可能主要是被动扩散。我们还在体外研究中证明：(1)活跃的K^+吸收发生在小鼠回肠中，(2)活跃的K^+吸收和分泌发生在小鼠远端结肠中。β -肾上腺素能激动剂和膳食钾负荷可增强远端结肠活跃的K^+分泌。此外，负责活性K^+吸收的结肠H，K- atp酶被多种瓦沙因样物质抑制。最后，醛固酮可促进结肠K^+的分泌，但对K^+的吸收无促进作用。

Potassium is one of the most abundant cation in the body, and plays a variety of physiological functions. This study aimed at elucidating the cellular mechanisms and regulation of intestinal K^+ transport. The results showed that; (1)in human study, urinary potassium excretion after potassium intake or potassium injection was accompanied by an increase in blood K^+, (2)in rat study using polyethylene glycol as an non-absorbable marker, ingested K^+ is absorbed mostly in the proximal jejunum probably mainly by passive diffusion. We have also demonstrated in in vitro studies that (1)active K^+ absorption occurs in the mouse ileum, (2)both active absorption and secretion of K^+ occur in the mouse distal colon. The active K^+ secretion in the distal colon was enhanced by beta-adrenergic agonists and dietary K load. In addition, the colonic H,K-ATPase responsible for active K^+ absorption was inhibited by a variety of ouabain-like substances. Finally, the colonic K^+ secretion was enhanced by aldosterone while the K^+ absorption was not enhanced.