DCT & Collecting duct

Dr.Ahsan Ashfaq
Assistant Professor Physiology
L.N.M.C
 Learning objectives

• By the end of this lecture students should be

able to.
• Describe segments of DCT and their role in
urine formation.
• Describe Collecting tubules
• Regulation of tubular reabsorption
• Hormonal control of tubular reabsorption
Tubular Reabsorption- Over View
 DCT
A portion of kidney nephron between
the loop of Henle and the collecting duct
system
 Structure

• Lined by simple cuboidal epithelium

• Basal membrane invaginations

• Numerous MT
Functions of the Distal Convoluted Tubule

• Reabsorbs Na+ ions and secrete H+ and K+

ions into the tubular fluid

• Plays an important role in acid-base balance

• Relatively impermeable to water

Functions of the Distal Convoluted Tubule

• Facultative reabsorption of water- ADH

• Secretes ammonium ions and some drugs

• Forms part of the juxtaglomerular apparatus

 Distal Tubule

• Thick ascending limb of the loop of Henle

empties into the distal tubule

• Impermeable to water and urea

• Referred to as the diluting segment

 Parts of Distal Tubule

• Two parts:

1-Early distal convoluted tubule (DCT1)

2-Late distal convoluted tubule (DCT2)

 Early distal tubule
Reabsorbs ~5 % of
the filtered load

Reabsorbs sodium,
chloride, calcium,
and magnesium

Impermeable to
water and urea
 Early distal tubule
• The excretion of Ca2+ - regulated in this part
of the nephron

• Parathormone and calcitriol -increase Ca2+

reabsorption
Mechanism of sodium chloride transport in
the early DCT
NaCl Co-transporter - moves NaCl from the
tubular lumen into the cell

Na-K ATPase pump- transports Na+ out of the cell

across the basolateral membrane

Cl- diffuses out of the cell into the renal

interstitial fluid via chloride channels

Thiazide diuretics - inhibit the NaCl co-transporter

 Mechanism of sodium chloride
transport in the early distal tubule
Late Distal tubule and cortical collecting tubule

The second half of the distal tubule and cortical collecting tubule
have similar fundamental characteristics being composed of
 Principal cells which reabsorb Na+ and Cl-and secrete K
 The P cell activity depends upon the activity of NaKATPase pump in each cell
basolateral membrane
 This pump maintains a low sodium concentration inside the cell
 The secretion of K involves two steps;
a) K enters the cell b/c of NaKATPase pump which maintains high
intracellular K conc.
b) once in the cell K diffuses down its conc. gradient across the luminal
membrane into the tubular fluid
Principal Cell
 Intercalated (I )cells

 Intercalated (I )cells reabsorb K + and secrete H +

 Hydrogen ion secretion by interclated cells is mediated by hydrogen ATPase
transport mechanism
 Hydrogen is generated by Carbonic anhydrase acting on CO2 and H2O to form
H2CO3

CO2 + H2O CA H2CO3

H2CO3 H + HCO3
Carbonic acid then dissociates into H+ & HCO3. H+ are then secreted into
tubular lumen and for each H+ secreted a HCO3 becomes available for
resorption across the basolateral membrane The I cells also reabsorb K+ ions
Intercalated Cell
 Characteristics of LDT & CCT
• The tubular membranes of both segments are almost
impermeable to urea collecting duct excretion
• Both segments reabsorb Na+, the rate controlled by hormones
aldosterone
• Secrete K+ which is also controlled by aldosterone & K+
concentration
• The I cells secrete H+ ions by an action Hydrogen ATPase
pump. Thus I cells play important role in acid base regulation
of the body fluids
• The permeability of these segments to H2O is controlled by
ADH (Vasopression) which renders these segments permeable
to H2O
 Medullary Collecting Duct

• MCD reabsorb less than 10 % filtered load of H2O & Na+ but
they are the final site for reabsorption and play an extremely
important role in determining the final urine output of H2O &
solutes
• MCD are lined by cuboidal epithelial cells which have smooth
surface and few mitochondria
1. The permeability of H2O is controlled by ADH
2. Permeable to urea therefore urea is reabsorbed into
medullary interstitium
3. It is capable of secreting H+ ions against a large concentration
(as in cortical collecting duct- CCT)
Reabsorption In Distal Tubule & Collecting Duct
 Regulation of Tubular Reabsorption
• Multiple neurons, hormonal, local control mechanism and
GFR controls tubular reabsorption.
• An important feature of tubular reabsorption is that excretion
of H2O and solutes can be independently controlled especially
through hormonal controls
1. Glomerulo-tubular balance represents the ability of the
tubule to ↑es its reabsorption rate in response to greater
tubular load.
↑ in GFR ↑ tubular reabsorption in proportion to the rise in
GFR
2. Peritubular capillary and renal interstitial fluid physical forces
alter tubular reabsorption of the 125 ml/min GFR,
approximately 124 ml/min is reabsorbed in peritubular
capillaries
 Regulation of Tubular Reabsorption

3. Filtration fraction (GFR/Renal plasma fluid) = An ↑ in filtration fraction tend

to raise peritubular capillary reabsorption rate.
4. ↑ed Arterial Pressure ↓es tubular reabsorption
• Even small ↑es in arterial pressure can raise the urinary excretion rates of
Na+ & H2O, phenomena that are known as Pressure Natriuresis & Pressure
Diuresis respectivley
a) ↑ed arterial pressure causes slight elevation in renal blood flow and GFR
(180 mmHg-60 mmHg will change slightly due to auto regulatory
mechanism)
↑ed arterial pressure raises peritubular capillary hydrostatic pressure
especially in Vasa Recta this in turn ↓es peri tubular capillary reabsorption
which causes leakage of Na into the lumen of the tubule thereby ↓ing the
net Na and H2O reabsorption resulting into ↑ed urine output
b) ↑ed arterial pressure also ↓es Angiotensin II formation ↓es
Na+ & H2O reabsorption
 Hormonal control of Tubular reabsorption

1. Aldosterone: ↑es Na+ reabsorption & ↑K+ secretion acts

mainly on Principal cells & stimulates Na-K ATPase pump
Addison’s Disease: No Aldosterone- there is marked loss of
Na+ & great ↑ in K+
Conn’s Syndrome: ↑ aldosterone will cause Na+ retention &
K+ depletion
2. Angiotensin II: ↑es Na+ & H2O reabsorption
a. Directly stimulates Na+ reabsorption at PCT
b. Efferent arteriolar constrictor
c. Stimulates aldosterone secretion
 Hormonal control of Tubular reabsorption
3. ADH ↑ H2O reabsortpion: Distal tubule & collecting ducts are
impermeable to H2O in the absence of ADH. However, less
than 10% H2O is reabsorbed under the action of ADH
4. Atrial Natriuretic Peptide (ANP) ↓es Na+ & H2O reabsorption:
Greater levels of this peptide hormone inhibit reabsorption
of H2O and Na+ from renal tubules causing greater excretion
of Na+ and H2O
5. PTH ↑es Calcium reabsortion & ↓es Phosphate
reabsortpion:
a. ↑es reabsortpion of Calcium in the thick ascending segment
& distal tubule
b. It causes inhibition of phosphate reabsorption at PCT
 Hormonal control of Tubular reabsorption

6. Sympathetic stimulation ↑es Na+ reabsorption:

• Causes constriction of both afferent and efferent arterioles,
thereby reducing GFR & at the same time directly stimulating
PCT and ascending segment to reabsorb Na+, Renin release
and Angiotensin II formation
 Role of ADH
• ADH binds to specific V2 receptors in the late distal tubule and
collecting ducts, ↑ing the formation of cAMP and activating
protein kinases
• This in turn stimulates the movement of intracellular protein
called Aquaporin-2 (AQP-2) to the luminal side of the basement
membrane
• The molecules of AQP-2 cluster together and fuse with the cell
membrane by exocytosis to form water channels that permit
rapid diffusion of water through the cells
• When the concentration of ADH ↓es, the molecules of AQP-2
are shuttled back to the cell cytoplasm, thereby, removing the
water channels from the luminal membrane and ↓ing water
permeability
Role of ADH
THANK YOU