Ion Channels – Membrane Transport – Intergrative Physiology
Kidney International (1999) 56, 2160–2167; doi:10.1046/j.1523-1755.1999.00780.x
NH4+ secretion in inner medullary collecting duct in potassium deprivation: Role of colonic H+-K+-ATPase
Suguru Nakamura, Hassane Amlal, John H Galla and Manoocher Soleimani
Correspondence: Manoocher Soleimani, M.D., Division of Nephrology and Hypertension, University of Cincinnati, 231 Bethesda Avenue, MSB 5502, Cincinnati, OH 45267-0585, USA. E-mail:Manoocher.Soleiman@uc.edu
Received 28 October 1998; Revised 27 May 1999; Accepted 19 July 1999.
Abstract
NH4+ secretion in inner medullary collecting duct in potassium deprivation: Role of colonic H+-K+-ATPase.
Background
In K+ deprivation (KD), gastric (g) H+-K+-ATPase (HKA) is suppressed, whereas colonic (c) HKA is induced in the terminal inner medullary collecting duct (IMCD). We hypothesized that in KD, cHKA is induced and can mediate the secretion of NH4+.
Methods
Rats were sacrificed after 2, 3, 6, or 14 days on regular (NML) or K+-free (KD) diet. mRNA expression of HKA isoforms in terminal inner medulla was examined and correlated with NH4+ secretion in perfused IMCD in vitro.
Results
Urinary NH4+ excretion increased after K+-free diet for six days. In terminal inner medulla, cHKA expression was strongly induced, whereas gHKA expression was decreased. NH4+ secretion increased by 62% in KD (JtNH4+ 0.57 vs. 0.92 pmol/min/mm tubule length, P < 0.001). Ouabain (1 mM) in perfusate inhibited NH4+ secretion in KD by 45% (P < 0.002) but not in NML. At luminal pH 7.7, which inhibits NH3 diffusion, NH4+ secretion in IMCD was 140% higher in KD (0.36 vs. 0.15, P < 0.03) and was sensitive to ouabain. ROMK-1 mRNA expression was induced in parallel with cHKA in inner medulla.
Conclusions
These data suggest that in KD, cHKA replaces gHKA and mediates enhanced secretion of NH4+ (and H+) into the lumen facilitated by K+ recycling through ROMK-1.
Keywords:
acid-base transporters, potassium depletion, collecting duct, proximal tubular acidosis, sodium reabsorption
