Abstract 043: Acute K+ Intake Does Not Reduce Renal Na-Cl Cotransporter Phosphorylation during Chronic AngII Hypertension
In Sprague Dawley (SD) rats, a single K+ rich meal provokes a 50% decrease in DCT Na-Cl cotransporter phosphorylation (NCCp) which shifts Na+ reabsorption downstream for reabsorption by CCD ENaC which drives a homeostatic increase in K+ secretion. During Ang II dependent hypertension, DCT NCCp increases 2-4 fold as does NCC mediated Na+ reabsorption. Motivated by these two recent findings, we tested the hypothesis that NCCp elevated by AngII hypertension (400 ng AngII/kg/min x 14 d in SD rats) could be reduced by a single K+ rich meal (3 hr 2% K meal). Three groups (n=5-6) of male SD rats were compared: 1) Untreated fed 0%K meal, 2) AngII infused fed 0%K meal, and 3) AngII infused fed 2%K meal. By immunoblot of renal cortical homogenates, AngII infusion increased the following 2-5 fold compared to the untreated group: NCC, NCCpS71, NCCpT53, NCCpS89, SPAK, SPAKpS373, and cleaved ENaC-gamma. A single 2%K meal did not reduce abundance or phosphorylation of NCC, SPAK or ENaC cleavage. Interestingly, the AngII infused rats exhibited signs of kaliuresis and K+ depletion compared to the untreated group: overnight urine K+ (UKV) was 4.3 +/- 0.1 vs. 2.3 +/- 0.3 mM, fasting plasma [K+] was 3.3 +/- 0.1 vs. 3.9 +/- 0.1 mEq in AngII vs. untreated, and while plasma [K+] climbed to 4.6 +/- 0.1 after the 2% K meal in AngII infused rats, UKV was not elevated compared to AngII rats fed a 0%K meal. The results indicate that a single K+ rich meal does not reduce NCCp in AngII infused rats, likely due to our finding that the AngII hypertension protocol provokes kaliuresis and K+ deficiency. Thus, the ingested K+ replenishes K+ stores and is not excreted. The results also suggest that the rise in NCCp during AngII hypertension may be, at least in part, a response aimed to reduce K+ excretion.
Author Disclosures: J. Han: None. D. Lee: None. L. Veiras: None. A.A. McDonough: None.
- © 2014 by American Heart Association, Inc.