Tubular Function

Examining reabsorption and secretion

Reabsorption in the PCT

Active transport of Na⁺, glucose, amino acids, and phosphates.

Water and Cl^- usually follow the charge and osmotic gradients

Reabsorption:

Active, therefore specificity and saturation

Amino acids --> neutral, acidic, and basic sites

Tmax (tubular maximum)

Energy from ion gradients (co-transport or symport) or ATP

As with any transport system, saturation occurs at high [plasma]_solute , giving a maximum rate of reabsorption or a T_max for each reabsorbed solute.

T_max depends upon # of transport sites

PCT & DCT Secretion

Organic Anions

Phenol Red

PAH

Creatinine

Penicillin

Acetazolamide

Furosemide

PCT & DCT Secretion

Organic Cations

Histamine

Norepinephrine

Quinine

Creatinine

QUESTION:

If secretion is a carrier mediated process, how does one explain the presence of transport sites for solutes not found in nature?

[Solute]_nephron

Blood = 300 mOsm

Bowman’s Capsule = 285 mOsm

PCT = 285 mOsm

Loop of Henle = 285 ---> 1,200 ---> 200 mOsm

DCT = 200 ---> 100 ---> 200 mOsm

CD = 200 ---> 285 ---> variable to 1,200 mOsm - [ADH] dependent

Antidiuretic Hormone
ADH (9 amino acids)

Also called vasopressin

8 Arginine or 8 Lysine Vasopressin

Released from posterior pituitary

In response to osmoreceptors in hypothalamus

Acts on Collecting Duct to increase water permeability

Causes decreased P & increased blood volume

Control of Blood Osmotic Pressure

Increased P ---> stimulate hypothalamus osmoreceptors

release of ADH into blood

Acts on CD to increase water permeability

Water diffuses from filtrate / urine into medulla and blood (vasa recta)

Why does water pass from urine / filtrate
into medullary space and blood?

COUNTERCURRENT
MECHANISMS

Multiplication

Exchange

Loops of Henle in Juxtamedullary Nephrons

MULTIPLIER EFFECT

COUNTERCURRENT EFFECT

ADH Dependent H₂O Permeability and Reabsorption

Diuretics

Osmotic, including water and non-reabsorbed solutes

Na⁺ - K⁺ ATPase inhibitors

Caffeine and theophylline

Furosamide

Alcohol - Inhibits ADH release

Increased renal BF, GFR & vasa recta BF

Regulation of Potassium Excretion

Two mechanisms:

[K⁺]_plasma

Aldosterone

Secreted from adrenal cortex

Regulation of Aldosterone

Stimuli

Elevated [K⁺]_plasma

Angiotensin II (via renin from juxtaglomerular cells)

Released from adrenal cortex

Action of Aldosterone

Acts on renal tubules to synthesize more Na⁺ - K⁺ ATPase

Increases Na⁺ reabsorption & K⁺ secretion and excretion

Atrial Natriuretic Peptide
(ANP)

Increases Na⁺ excretion by decreasing Na⁺ reabsorption

Decreases Aldosterone secretion

Decreases Renin secretion

= more water & Na⁺ excretion

Atrial Natriuretic Peptide
(ANP)

Released in response to artial stretch

due to increased blood volume and BP

Blood Volume Regulation

Decreased blood or extra-cellular fluid volume ---> increased renin

----> Increased renin & aldosterone

Increased blood or extra-cellular fluid volume ---> increased ANP

Calcium -- Phosphate
Relationships

Increased [Ca⁺⁺]_plasma must be accompanied by a decreased [HPO₄^-2]_plasma

Parathyroid Hormone
(PTH)

Parathyroid hormone (PTH) increases Ca⁺⁺ reabsorption and decreases HPO₄^-2 reabsorption

Increases HPO₄^-2 excretion and decreases Ca⁺⁺ excretion

PTH

Released in response to decreased plasma Ca⁺⁺