HYPERTONIA ÉS NEPHROLOGIA - eLitMed.hu

ABBREVIATIONS
CCD: cortical collecting duct
ENaC: epithelial Na + channel
Po : open probability
ROMK: rat outer medullary K channel
RT-PCR: reverse transcriptase-polymerase chain reaction
SK channel: secretory K channel
TALH: thick ascending limb of Henle’s loop
TEA: tetraethylammonium
ÖSSZEFOGLALÓ KÖZLEMÉNYEK
Ontogeny of potassium transport in the distal
nephron
Lisa M. Satlin, M.D.
Associate Professor
Division of Nephrology Department of Pediatrics and Medicine, Mount Sinai School of Medicine, New York, N.Y., U.S.A.
Correspondence
Lisa M. Satlin, M.D. phone: (212) 241-7148
Box 1664 fax: (212) 426-1972
Mount Sinai School of Medicine e-mail: lisa.satlin@mssm.edu
One Gustave L. Levy Place
SUMMARY Kidneys of full-term newborn humans and animals conserve K + , a condition essential for somatic growth.
The cortical collecting duct (CCD) within the distal nephron is uniquely adapted to retain total body K + early in life. CCDs
isolated from newborn rabbits and microperfused in vitro show no net K + secretion until after the third week of life; in
contrast, segments isolated from adult animals secrete net K + at high rates. The magnitude and direction of net K +
transport in the CCD reflect the balance of opposing fluxes of K + secretion and K + absorption, mediated by principal and
intercalated cells, respectively. Evidence now indicates that the limited capacity of the CCD for K + secretion early in life is
due a limited capacity of principal cells for K + secretion, due, at least in part, to a relative paucity of conducting apical K +
channels. A relative excess of K + absorption by intercalated cells may further reduce net urinary K + secretion. In fact,
fluorescent functional assays identify significant activity of apical H-K-ATPase, a pump which reabsorbs K + in exchange
for H, in neonatal intercalated cells. Under conditions prevailing in vivo, the balance of fluxes mediated by these two cell
types likely contributes to the relative K + retention characteristic of the neonatal kidney.
Key-words: potassium transport, neonatal kidney, distal nephron
Supported in part by NIH grant DK38470 and a Grant-in-Aid
from the American Heart Association.
HYPERTONIA ÉS NEPHROLOGIA 2002; 6 (1):3–15.
INTRODUCTION Total body K + content depends on the
balance between intake and output, the latter regulated
primarily by renal excretion. The kidneys of the healthy adult,
whose homeostatic goal is to remain in zero balance, are
responsible for the elimination of ~90% of the typical daily K +
intake of ~1 mEq per kilogram body weight per day; the
residual 10% of the daily K + load is lost through the stool (1).
However, clearance studies reveal that newborns consistently
demonstrate low baseline rates of urinary K + excretion, even
when corrected for the low glomerular filtration rate
prevailing early in life (2). The requirement of the growing
subject for K + conservation is reflected in the observation that
infants maintain a state of positive K + balance (2).
Within the fully differentiated nephron, the final renal
regulation of K + excretion occurs in the connecting and
collecting ducts (1; 3-10). Cortical collecting ducts (CCDs)
isolated from adult (8 weeks of age) rabbits and
microperfused in vitro at physiologic flow rates secrete net K +