Reabsorption & secretion Part - I

Tubular functions Formation of urine is the result of 2 major processes: 1) Glomerular filteration. 2) Tubular transport. Tubular transport: 1) Reabsorption. 2) Secretion.

Eff. Art. Filteration Reabsorption Secretion EX. Aff. Art. Peritub. Cap. Reabsorption Filteration Secretion EX. Renal pelvis, ureter

Summary of events that occur inside PCT Reabsorption of All filtered glucose, amino acids, vitamins, protein and Kreb’s cycle intermediates. Reabsorption of About 2/3 of filtered load of Na+ & water. Co-transport of K+, glucose, amino acids at 1st half of PCT. Absorption of CL- & secretion of H+ ions in 2nd half of PCT. Reabsorption & synthesis of NaHCO3. Remaining tubular fluid is isotonic (300 mosmol) but slightly acidic (pH<7.35).

Loop of Henle Descending LH: Ascending LH: Epithelium: Very thin endothelial –like cells. Permeability (high to water, hard to solutes) Ascending LH: Thin ascending LH: Presents only in long loops Epithelium: is Impermeable to water Permeable to solutes → allow Na reabsorption, and Urea secretion Thick ascending LH: Epithelium: Basolateral border rich in Na-K pump Apical border contain Na-K-2Cl transporter

20-25% Nacl 15% Water

Overall Functions of Distal Segment Final adjustment of urine formation. Reabsorption of 7-10% of filtered load of Na+. Reabsorption of 10-15% of filtered lead of water. Secretion of variable amount of H+ & K+. Major control site for Na+, K+, Ca2+ & acid-base balance of body. Many of these functions are controlled by hormones.

Characters of DCT Reabsorbs 4% of filtered load of Na+. NaCl is transported by a Na+ - Cl- transporter located at apical border. This transporter is inhibited by thiazide diuretics. The basolateral Na+- K+ ATPase together with that of thick ALH has highest activity of any nephron segment. The osmolarity of tubular fluid leaving DCT is 100 mOsm/L (i.e. more hypotonic)  so, the diluting segments of the nephron are: thick ALH and early DCT.

Principal cells (P-cells) Intercalated cells (I-cells) Collecting Ducts (CD) Each 8 DCTs unite together forming cortical CD that pass to medulla to form medullary CD that unite together forming minor calyces, then major calyces, then renal pelvis and finally the ureter. It is lined by: Principal cells (P-cells) Intercalated cells (I-cells) Predominate with few organells Less in number with more mitochondria, microvilli & cytoplasmic vesicles. Na+ reabsorption (controlled by Aldosterone) Water reabsorption (controlled by ADH) Involved in H+ secretion & HCO3- transport (also, found in DCT).

Renal Handling of Na+ Functions of Na+: Mechanism of Na+ reabsorption: Keeping of extracellular fluid volume & blood volume constant. Formation of RMP, action potential & conduction of nerve impulse. Mechanism of Na+ reabsorption: Na+ reabsorption is associated with transport of many substances as H2O, H+, glucose, amino acids, Cl-, Hco3- and with K+ excretion. In PCT (67-70%): At luminal border: Na+ is transported from lumen to inside cells by Facilitated diffusion. (Carrier mediated but no energy) according to: Concentration gradient. Electrical gradient (inside cell -70 mV & in lumen -3 mV). Helped by  surface area of brush border of cells of PCT & by carriers. Also, Na+ is transported paracellular.

Renal Handling of Na+ At baso-lateral border: Na+ is transported from cell to interstitium by Na+ - K+ ATPase pump (active). When K+ enters the cell. K+ diffuses back again to interstitium by concentration gradient and high permeability of cell membrane  maintains intracellular –ve to attract more Na+ to enter the cell (help Facilitated diffusion).

Na+ Handling

Transcellular and Paracellular Transport Transcellular Transport

Results of Na+ reabsorption in PCT: Reabsorption of 67-70% of water (obligatory). Due to: high osmolality created by Na+ & other ions reabsorption. Passive diffusion of Cl- in 2nd half of PCT. Due to:  Cl- concentration. Active co-transport of glucose, amino acids & bicarbonate. Due to: co-transport mechanism (two or more substances are carried by same carrier in same direction).

Renal Handling of Na+ In loop of Henle (20-25%): At thin descending part: It is the only part in the nephron in which Na+ is not reabsorbed. Fluid reaching medulla is hypertonic (freely permeable to H2O). At thin ascending part: passive Na+ reabsorption. At the thick ascending part: Na+ is reabsorbed by active co-transport protein carrier (1Na+, 1K+, 2 Cl-). Fluid leaving this thick part is hypotonic (poorly permeable to H2O).   In DCT & CD (8-10%): Na+ is actively reabsorbed in DCT in exchange with K+ or H+ by help of aldosterone.

Factors controlling Na+ reabsorption & excretion Amount of Na+ excreted per day may be as low as 1 mEq/day to as high as 400 mEq/day. 1- Amount of NaCL intake per day:  Intake   Na+ reabsorption & excretion. 2- Hormonal factors: A- Aldosterone: Most important in controlling Na+ reabsorption in kidney, intestine & sweat glands. Acts mainly on DCT (principal cells) & in collecting tubules.  Na+ reabsorption in exchange with K+ & H+   Na+ excretion.

B- Glucocorticoids (cortisol): Aldosterone like action in large doses.  Na+ & H2O reabsorption and  Na+ excretion in urine. C- Sex hormones (estrogens): Weak aldosterone - like action. So, contraceptive pills  edema. D- Atrial natriuretic peptide (ANP)   Na+ excretion. Acts by cGMP in DCT cells. ANP increases GFR   amount of filtered Na+.

Factors controlling Na+ reabsorption & excretion 3- ABP:  ABP above 180 mmHg   Na+ excretion (pressure diuresis). Independent on neither nervous nor hormonal factors.   4-Diuretics: Osmotic diuretics as mannitol→ ↓ Na+ reabsorption from PCT. Loop diuretics (Lasix) → ↓ Na+ reabsorption from Henle's loop. Aldactone → ↓ Aldosterone → ↓ Na+ reabsorption from DCT.

Renal Handling of Chloride The chief Extracellular anion. It equals 104 mEq/L. 99% of the filtered chloride is reabsorbed by: Active: in thick ascending part of Henel’s loop by 1Na+, 1K+, 2 Cl-. Passive: in PCT & CD secondary to Na+ reabsorption.