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Renal mechanisms driving K excretion after a K containing meal
Author(s) -
Rengarajan Srinivas,
Youn Jang H,
Lee Donna H.,
McDonough Alicia A
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1210.8
Subject(s) - reabsorption , endocrinology , medicine , chemistry , kaliuresis , excretion , renal cortex , meal , urine , distal convoluted tubule , urine osmolality , ketamine , kidney , natriuresis , anesthesia
We aimed to determine the molecular mechanisms leading to renal K excretion after an acute meal induced K load by studying ion transporter regulation. Method Male Sprague Dawley rats (n=8) were fasted overnight with free access to water and then fed a meal with no K + (0K) or 2% K + (2K) for 3 hours in metabolic cages. Urine was collected and after anesthesia (ketamine‐xylazine), blood was sampled, kidneys removed and cortex and medulla homogenates were prepared. Transporter abundance and phosphorylation were assessed by quantitative immunoblots with specific antibodies. Results A single K rich meal increased plasma [K + ] within the normal range in the 2K versus 0K group: 5.18±0.16mEq versus 4.01±0.12mEq (p<0.01), and sharply increased urine K + in the 2K versus 0K group: 713±48 versus 55±15μmol (p<0.01). Urine volume tended to increase in the 2K versus 0K group: 3.63±0.16 versus 1.97±0.54ml/3 hr, but urine Na was unchanged. Cortical NCC, NCC‐P and SPAK‐P abundance were decreased by 24±4% (p<0.01), 63±4% (p<0.01) and 38±5% (p<0.01) respectively in 2K versus 0K rats. NHE3, ENaC and ROMK were unchanged by 2K diet feeding. We postulate that the kaliuresis can be explained by a decrease in distal convoluted tubule (DCT) Na which would drive more Na to the cortical collecting duct (CCD) where Na reabsorption drives K secretion, analogous to the effect of an NCC inhibitor. Research support: NIH DK083785