Halperin Mitchell L, Cheema-Dhadli Surinder, Lin Shih-Hua, Kamel Kamel S
Renal Division, St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada.
Curr Opin Nephrol Hypertens. 2006 Jul;15(4):430-6. doi: 10.1097/01.mnh.0000232884.73518.9c.
Regulation of potassium (K) excretion was examined in an experimental setting that reflects the dietary conditions for humans in Paleolithic times (high, episodic intake of K with organic anions; low intake of NaCl), because this is when major control mechanisms were likely to have developed.
The major control of K secretion in this setting is to regulate the number of luminal K channels in the cortical collecting duct. Following a KCl load, the K concentration in the medullary interstitial compartment rose; the likely source of this medullary K was its absorption by the H/K-ATPase in the inner medullary collecting duct. As a result of the higher medullary K concentration, the absorption of Na and Cl was inhibited in the loop of Henle, and this led to an increased distal delivery of a sufficient quantity of Na to raise K excretion markedly, while avoiding a large natriuresis. In addition, because K in the diet was accompanied by 'future' bicarbonate, a role for bicarbonate in the control of K secretion via 'selecting' whether aldosterone would be a NaCl-conserving or a kaliuretic hormone is discussed.
This way of examining the control of K excretion provides new insights into clinical disorders with an abnormal plasma K concentration secondary to altered K excretion, and also into the pathophysiology of calcium-containing kidney stones.
在一种反映旧石器时代人类饮食状况（高钾且间歇性摄入有机阴离子；低钠摄入）的实验环境中研究钾（K）排泄的调节，因为主要的控制机制可能就是在这个时期形成的。
在这种情况下，钾分泌的主要控制方式是调节皮质集合管腔膜钾通道的数量。摄入氯化钾后，髓质间质中的钾浓度升高；髓质钾的可能来源是其被内髓集合管中的H/K-ATP酶吸收。由于髓质钾浓度升高，亨利氏袢中钠和氯的吸收受到抑制，这导致向远曲小管输送足够量的钠增加，从而显著提高钾排泄，同时避免大量钠利尿。此外，由于饮食中的钾伴随着“未来的”碳酸氢盐，还讨论了碳酸氢盐通过“选择”醛固酮是作为保钠还是排钾激素来控制钾分泌的作用。
这种研究钾排泄控制的方法为因钾排泄改变导致血浆钾浓度异常的临床疾病以及含钙肾结石的病理生理学提供了新的见解。
