title: K+ supplementation increases muscle [Na+-K+-ATPase] and improves extrarenal K+ homeostasis in rats.
abstract: Effects of K+ supplementation (approximately 200 mmol KCl/100 g chow) on plasma K+, K+ content, and Na+-K+-adeonsinetriphosphatase (ATPase) concentration ([Na+-K+-ATPase]) in skeletal muscles as well as on extrarenal K+ clearance were evaluated in rats. After 2 days of K+ supplementation, hyperkalemia prevailed (K+-supplemented vs. weight-matched control animals) [5.1 +/- 0.2 (SE) vs. 3.2 +/- 0.1 mmol/l, P < 0.05, n = 5-6], and after 4 days a significant increase in K+ content was observed in gastrocnemius muscle (104 +/- 2 vs. 97 +/- 1 micromol/g wet wt, P < 0.05, n = 5-6). After 7 days of K+ supplementation, a significant increase in [3H] ouabain binding site concentration (344 +/- 5 vs. 239 +/- 8 pmol/g wet wt, P < 0.05, n = 4) was observed in gastrocnemius muscle. After 2 wk, increases in plasma K+, K+ content, and [3H]ouabain binding site concentration in gastrocnemius muscle amounted to 40, 8, and 68% (P < 0.05) above values observed in weight-matched control animals, respectively. The latter change was confirmed by K+-dependent p-nitrophenyl phosphatase activity measurements. Fasting for 1 day reduced plasma K+ and K+ content in gastrocnemius muscle in rats that had been K+ supplemented for 2 wk by 3.1 +/- 0.3 mmol/l (P < 0.05, n = 5) and 15 +/- 2 micromol/g wet wt (P < 0.05, n = 5), respectively. After induction of anesthesia, arterial plasma K+ was measured during intravenous KCl infusion (0.75 mmol KCl x 100 g body wt(-1) x h(-1)). The K+-supplemented fasted group demonstrated a 42% (P < 0.05) lower plasma K+ rise, associated with a significantly higher increase in K+ content in gastrocnemius muscle of 7 micromol/g wet wt (P < 0.05, n = 5) compared with their control animals. In conclusion, K+ supplementation increases plasma K+, K+ content, and [Na+-K+-ATPase] in skeletal muscles and improves extrarenal K+ clearance capacity.
authors.affiliation: Department of Medicine B, The Heart Centre, Rigshospitalet, National University Hospital, Copenhagen, Denmark.
authors.forename: H
authors.initials: H
authors.lastname: Bundgaard
authors.forename: T A
authors.initials: TA
authors.lastname: Schmidt
authors.forename: J S
authors.initials: JS
authors.lastname: Larsen
authors.forename: K
authors.initials: K
authors.lastname: Kjeldsen
mesh_terms: D000818:Animals; D001834:Body Water / Q000378:metabolism; D004032:Diet; D004791:Enzyme Inhibitors; D005260:Female; D006706:Homeostasis / Q000187:drug effects / Q000502:physiology*; D007262:Infusions, Intravenous; D018482:Muscle, Skeletal / Q000187:drug effects / Q000201:enzymology* / Q000378:metabolism; D009392:Nephrectomy; D010042:Ouabain; D011188:Potassium / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology*; D011189:Potassium Chloride / Q000008:administration & dosage / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012982:Sodium, Dietary / Q000494:pharmacology; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D015854:Up-Regulation / Q000187:drug effects
chemical_list: D004791:Enzyme Inhibitors; D012982:Sodium, Dietary; D010042:Ouabain; D011189:Potassium Chloride; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium