Page 175 - Color_Atlas_of_Physiology_5th_Ed._-_A._Despopoulos_2003

Reabsorption of Na and Cl – ! In the distal convoluted tubule, DCT (! B8),
+
Na is reabsorbed via the thiazide-sensitive co-
+
About 99% of the filtered load of Na is reab- transporter TSC, an electroneutral Na -Cl -
+
+
sorbed (ca. 27 000 mmol/day), i.e., the frac- symport carrier (! p. 172).
+
tional excretion of Na (FE Na) is about 1%. The ! In principal cells of the connecting tubule
+
precise value of FE Na needed (range 0.5 to 5%) is and collecting duct (! B9), Na exits the lumen
+
regulated by aldosterone, atriopeptin (ANF) via Na channels activated by aldosterone and
and other hormones (! p. 170). antidiuretic hormone (ADH) and inhibited by
Sites of Na reabsorption. The reabsorption prostaglandins and ANF (! p. 170).
+
Kidneys, Salt, and Water Balance luminal Na conc. remains constant (! p. 166). brane (Na -K -ATPase), the associated trans-
+
+
Since these four passive Na transport steps in
of Na occurs in all parts of the renal tubule and
the luminal membrane are serially connected
collecting duct. About 65% of the filtered Na is
+
reabsorbed in the proximal tubule, while the
to active Na transport in the basolateral mem-
+
+
+
+
Another 25% is reabsorbed in the loop of Henle,
+
epithelial Na reabsorption is also active. This
+
makes up about /3 of the Na reabsorption in
conc. drops sharply;
+
where luminal Na
1
the proximal tubule, and 1 ATP molecule is
! p. 157 D, columns 2 and 3). The distal convo-
+
ions absorbed
luted tubule and collecting duct also reabsorb
consumed for each 3 Na
+
(! p. 26). The other /3 of proximal sodium re-
Na . The latter serves as the site of hormonal
2
absorption is passive and paracellular.
+
fine adjustment of Na excretion.
+
+
+
Mechanisms of Na reabsorption. Na -K -
+
ATPase pumps Na ions out of the cell while
LPTP in the mid and late proximal tubule (! B5) and
+
in the loop of Henle (! B7) drives Na and other cati-
7 conveying K + ions into the cell (! A and + Two driving “forces” are responsible for this: (1) the
p. 156), thereby producing a chemical Na
ons onto the blood side of the epithelium. (2) Sol-
+
gradient (! A2). Back diffusion of K (! A3) vent drag (! p. 24): When water is reabsorbed, sol-
also leads to the development of a membrane utes for which the reflection coefficient ! 1 (includ-
+
potential (! A4). Both combined result in a ing Na ) are “dragged along” due to friction forces
(like a piece of wood drifts with flowing water). Since
high electrochemical Na gradient that pro- driving forces (1) and (2) are indirect products of
+
vides the driving “force” for passive Na influx, Na -K -ATPase, the energy balance rises to about 9
+
+
+
the features of which vary in the individual Na per ATP molecule in the proximal tubule (and to
+
nephron segments (! B). about 5 Na per ATP molecule in the rest of the kid-
+
+
! In the proximal tubule, Na ions diffuse pas- ney).
+
sively from the tubule lumen into the cells via On the basolateral side, Na ions exit the proximal
+
+
+
+
+
(a) the electroneutral Na /H exchanger type 3 tubule cell via Na -K -ATPase and an Na -3 HCO 3 – +
symport carrier (! p. 174). In the latter case, Na
(NHE3), an Na /H -antiport carrier for elec- exits the cell via tertiary active transport as second-
+
+
+
+
troneutral exchange of Na for H (! B1, p. 29 ary active secretion of H (on the opposite cell side)
+
B4 and p. 174) and (b) various Na symport car- results in intracellular accumulation of HCO 3 . –
+
riers for reabsorption of D-glucose etc. (! B1 The fractional Cl excretion (FE Cl) ranges from
-
and p. 158). Since most of these symport car- 0.5% to 5%. About 50% of all Cl reabsorption
–
riers are electrogenic, the luminal cell mem- occurs in the proximal tubule. The early proxi-
brane is depolarized, and an early proximal mal LNTP drives Cl – through paracellular
lumen-negative transepithelial potential (LNTP) spaces out of the lumen (! B3). The reabsorp-
develops. tion of Cl lags behind that of Na and H 2O, so
+
–
! In the thick ascending limb (TAL) of the loop the luminal Cl conc. rises. As a result, Cl starts
–
–
+
of Henle (! B6), Na is reabsorbed via the to diffuse down its chemical gradient para-
bumetanide-sensitive co-transporter BSC, a cellularly along the mid and late proximal
+
Na -K -2 Cl – symport carrier (! p. 172). Al- tubule (! B4), thereby producing a LPTP (re-
+
though BSC is primarily electroneutral, the ab- versal of potential, ! B5). At the TAL and the
sorbed K + recirculate back to the lumen DCT, Cl enters the cells by secondary active
–
+
through K channels. This hyperpolarizes the
luminal membrane, resulting in the develop- transport and exits passively through ADH-ac-
–
162 ment of a lumen-positive transepithelial tivated basolateral Cl channels (! B6, 8).
potential (LPTP).
Despopoulos, Color Atlas of Physiology © 2003 Thieme
All rights reserved. Usage subject to terms and conditions of license.