{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T20:56:01Z","timestamp":1792270561740,"version":"4.4.0"},"reference-count":27,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2004,3]]},"abstract":"<jats:p> Apical potassium recycling is crucial for salt transport by the thick ascending limb (TAL). Loss-of-function mutations in the K channel, ROMK (Kir1.1; KCNJ1), cause Bartter syndrome, a genetically heterogeneous disorder characterized by severe reduction in salt absorption by the TAL, Na wasting, polyuria, and hypokalemic alkalosis. ROMK(-\/-) null mice exhibit a Bartter phenotype and lack the small-conductance (30-pS) apical K channel (SK) in the TAL. However, a distinct 70-pS K channel can also significantly contribute to the apical conductance of TAL. We now examine the effect of ROMK deletion on the functional expression of the 70-pS K channel in the TAL. Functional expression of the 70-pS K channel was low [average channel acitivty ( NP<jats:sub>o<\/jats:sub>) = 0.02] in ROMK(+\/+) mice on a control K diet but increased to 0.27 by high-K intake for 2 wk. In contrast, the high-K diet decreased NP<jats:sub>o<\/jats:sub> of SK by \u223c30%, from 2.04 to 1.44. In ROMK heterozygous (+\/-) mice on a control K diet, SK activity was about one-half of that observed in ROMK(+\/+) mice (0.95 vs. 2.04). The high-K diet also reduced SK activity in ROMK(+\/-) mice by \u223c40% (from 0.95 to 0.55) but increased NP<jats:sub>o<\/jats:sub> of the 70-pS K channel from 0 to 0.09 in ROMK(+\/-) mice. This corresponds to \u223c30% of channel activity ( NP<jats:sub>o<\/jats:sub> = 0.27) observed in ROMK(+\/+) mice. Neither the 70-pS nor the 30-pS K channels were observed in TAL cells from ROMK(-\/-) mice on either the normal or high-K diets. Thus functional expression of the 70-pS K channel is enhanced by increasing dietary K and requires expression of ROMK. It is likely that ROMK forms a critical subunit of the 70-pS K channel, accounting for the loss of apical K secretory channel activity in ROMK Bartter syndrome. <\/jats:p>","DOI":"10.1152\/ajprenal.00305.2003","type":"journal-article","created":{"date-parts":[[2004,2,3]],"date-time":"2004-02-03T15:35:42Z","timestamp":1075822542000},"page":"F490-F495","source":"Crossref","is-referenced-by-count":56,"title":["ROMK is required for expression of the 70-pS K channel in the thick ascending limb"],"prefix":"10.1152","volume":"286","author":[{"given":"Ming","family":"Lu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tong","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qingshang","family":"Yan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wenhui","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gerhard","family":"Giebisch","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven C.","family":"Hebert","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1007\/BF00373623"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1995.268.6.F1132"},{"key":"REF3","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1998.274.3.H817"},{"key":"REF4","doi-asserted-by":"crossref","unstructured":"Greger R, Bleich M, and Schlatter E. Ion channels in the thick ascending limb of Henle's loop. Renal Physiol Biochem 13: 37-50, 1990.","DOI":"10.1159\/000173346"},{"key":"REF5","doi-asserted-by":"publisher","DOI":"10.1007\/BF00584588"},{"key":"REF6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2001.280.2.F223"},{"key":"REF7","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.2001.281.4.C1188"},{"key":"REF8","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.119.1.33"},{"key":"REF9","doi-asserted-by":"publisher","DOI":"10.1097\/00041552-200309000-00008"},{"key":"REF10","doi-asserted-by":"publisher","DOI":"10.1007\/BF01868439"},{"key":"REF11","unstructured":"Hebert SC and Wang WH. Structure and function of the low conductance KATP channel, ROMK. Wien Klin Wochenschr 109: 471-476, 1997."},{"key":"REF12","doi-asserted-by":"publisher","DOI":"10.1038\/362031a0"},{"key":"REF13","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M205627200"},{"key":"REF14","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.116.2.299"},{"key":"REF15","doi-asserted-by":"publisher","DOI":"10.1159\/000025957"},{"key":"REF16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1998.274.5.F946"},{"key":"REF17","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M206644200"},{"key":"REF18","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.108.6.537"},{"key":"REF19","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.6.F916"},{"key":"REF20","doi-asserted-by":"crossref","unstructured":"Palmer LG, Choe H, and Frindt G. Is the secretory K channel in the rat CCT ROMK? Am J Physiol Renal Physiol 273: F404-F410, 1997.","DOI":"10.1152\/ajprenal.1997.273.3.F404"},{"key":"REF21","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1999.277.5.F805"},{"key":"REF22","doi-asserted-by":"publisher","DOI":"10.1038\/ng1096-152"},{"key":"REF23","doi-asserted-by":"crossref","unstructured":"Wald H, Garty H, Palmer LG, and Popovtzer MM. Differential regulation of ROMK expression in kidney cortex and medulla by aldosterone and potassium. Am J Physiol Renal Physiol 275: F239-F245, 1998.","DOI":"10.1152\/ajprenal.1998.275.2.F239"},{"key":"REF24","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.physiol.59.1.413"},{"key":"REF25","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.2000.278.1.F165"},{"key":"REF26","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.ph.54.030192.000501"},{"key":"REF27","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1994.267.4.F599"}],"container-title":["American Journal of Physiology-Renal Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.physiology.org\/doi\/pdf\/10.1152\/ajprenal.00305.2003","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T17:31:13Z","timestamp":1567963873000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.physiology.org\/doi\/10.1152\/ajprenal.00305.2003"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2004,3]]},"references-count":27,"journal-issue":{"issue":"3","published-print":{"date-parts":[[2004,3]]}},"alternative-id":["10.1152\/ajprenal.00305.2003"],"URL":"https:\/\/doi.org\/10.1152\/ajprenal.00305.2003","relation":{},"ISSN":["1931-857X","1522-1466"],"issn-type":[{"value":"1931-857X","type":"print"},{"value":"1522-1466","type":"electronic"}],"subject":[],"published":{"date-parts":[[2004,3]]}}}