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Скачать или смотреть HORMONAL CONTROL OF TUBULAR REABSORPTION Mastering QUIZ-10

  • Dr Sheen Medical lectures
  • 2025-12-28
  • 3
HORMONAL CONTROL OF TUBULAR REABSORPTION Mastering QUIZ-10
kidney tubular reabsorptionhormonal regulation kidneysaldosterone sodium reabsorptionangiotensin II water retentionADH water permeabilitynatriuretic peptides ANP BNPparathyroid hormone calciumrenal hormones functionsbody fluid balanceelectrolyte regulationaldosterone potassium secretionangiotensin II efferent constrictionADH aquaporin-2ANP volume expansionPTH phosphate inhibitionperitubular capillary dynamicsdiabetes insipidus ADH absence
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Hormonal Control of Kidney Tubular Reabsorption
The kidneys maintain balanced body fluids by precisely controlling how much water and salts (solutes like sodium, potassium) they reabsorb from filtered fluid back into the blood. This happens in tiny tubes called tubules. Hormones act like signals to adjust reabsorption for different needs, allowing the kidneys to handle changes in diet or body conditions without disrupting overall balance. For example, they can increase potassium excretion while keeping sodium steady.
Key Hormones and Their Roles
Aldosterone: Produced by the adrenal glands, it's a major regulator. It boosts reabsorption of sodium (Na), chloride (Cl), and bicarbonate (HCO3) in the collecting tubules, while increasing secretion of potassium (K) and hydrogen (H) ions. This helps retain salt and water during low volume, but excretes excess K to prevent buildup.
Triggers: High blood K or angiotensin II (from low blood pressure).
Effects: Stimulates pumps and channels in tubule cells for Na uptake and K release.
Problems: Too little (Addison's disease) causes Na loss and K accumulation. Too much (Conn's syndrome) leads to high blood pressure, low K, and alkalosis (too basic blood).
Angiotensin II: A powerful hormone for salt retention, activated during low blood pressure, dehydration, or salt loss (e.g., sweating).
How it works:
Stimulates aldosterone release.
Constricts outgoing (efferent) kidney blood vessels, lowering pressure in surrounding capillaries. This reduces "backleak" of fluid into tubules and increases reabsorption, especially in proximal tubules.
Directly activates Na pumps and exchangers in tubules (proximal, loop of Henle, distal, collecting).
Result: Retains Na and water to restore volume and pressure, while allowing waste like urea to be excreted.
Antidiuretic Hormone (ADH, or Vasopressin): Focuses on water conservation during dehydration.

Action: Increases water permeability in distal and collecting tubules by inserting water channels (aquaporin-2) via cell signaling (cAMP pathway).
Absence: Causes diabetes insipidus—kidneys can't reabsorb water, leading to excessive dilute urine.
Natriuretic Peptides (ANP and BNP): Released by the heart when blood volume is high (e.g., heart stretch from overload).

ANP from atria; BNP from ventricles.
Effects: Inhibit Na and water reabsorption in collecting ducts; dilate kidney vessels; reduce renin (lowers angiotensin II and aldosterone).
Outcome: Increases urine output to reduce volume and pressure, helpful in heart failure.
Parathyroid Hormone (PTH): Mainly for calcium balance.

Boosts Ca reabsorption in distal tubules; reduces phosphate (PO4) reabsorption in proximal tubules; increases magnesium (Mg) in loop of Henle.
Supporting Concepts
Peritubular Dynamics: Blood vessels around tubules influence reabsorption. High pressure or low protein concentration in capillaries increases backleak through cell junctions, reducing net reabsorption (see figure example).
Overall Goal: These hormones allow flexible adjustments—e.g., more Na retention during low intake—keeping body fluids stable without retaining wastes.
In summary, hormones fine-tune kidney function like a smart thermostat, responding to body signals for optimal fluid and electrolyte harmony. This prevents issues like swelling, weakness, or irregular heartbeats from imbalances.

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