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Questions and Answers
What percentage of filtered urea is reabsorbed in the proximal tubules?
What percentage of filtered urea is reabsorbed in the proximal tubules?
What occurs to filtered peptides in the proximal tubule?
What occurs to filtered peptides in the proximal tubule?
Which mechanism is used for the uptake of low molecular weight proteins in the proximal tubules?
Which mechanism is used for the uptake of low molecular weight proteins in the proximal tubules?
Which of the following proteins is not a low-molecular-weight filtered protein mentioned in the content?
Which of the following proteins is not a low-molecular-weight filtered protein mentioned in the content?
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What is the main effect of increasing molecular weight from 10 kDa to 70 kDa on filtration in the proximal tubule?
What is the main effect of increasing molecular weight from 10 kDa to 70 kDa on filtration in the proximal tubule?
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What percentage of energy spent by the kidney is used for the Na/K ATPase pump?
What percentage of energy spent by the kidney is used for the Na/K ATPase pump?
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What role does the Na/K ATPase pump play in sodium concentration in the kidney?
What role does the Na/K ATPase pump play in sodium concentration in the kidney?
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Which mechanism allows for the passive movement of water in the nephron?
Which mechanism allows for the passive movement of water in the nephron?
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What percentage of filtered water is passively reabsorbed by the end of the proximal tubule?
What percentage of filtered water is passively reabsorbed by the end of the proximal tubule?
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What enhances the return of filtered water to the plasma in the kidney?
What enhances the return of filtered water to the plasma in the kidney?
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How does active sodium reabsorption affect the reabsorption of urea?
How does active sodium reabsorption affect the reabsorption of urea?
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What is the main pathway for water reabsorption in the proximal tubule?
What is the main pathway for water reabsorption in the proximal tubule?
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What happens to the concentration of sodium in the tubular lumen as it moves into the tubular cell?
What happens to the concentration of sodium in the tubular lumen as it moves into the tubular cell?
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What is the acute effect of aldosterone on sodium reabsorption?
What is the acute effect of aldosterone on sodium reabsorption?
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Which process is NOT involved in adjusting the amount of sodium excreted by the kidneys?
Which process is NOT involved in adjusting the amount of sodium excreted by the kidneys?
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What is the role of aldosterone in the distal convoluted tubule?
What is the role of aldosterone in the distal convoluted tubule?
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How is sodium filtered in the kidneys primarily controlled?
How is sodium filtered in the kidneys primarily controlled?
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What occurs as a chronic effect of aldosterone?
What occurs as a chronic effect of aldosterone?
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Where is the majority of potassium (K) predominantly found in the body?
Where is the majority of potassium (K) predominantly found in the body?
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What is the effect of the renin-angiotensin-aldosterone system (RAAS) on sodium?
What is the effect of the renin-angiotensin-aldosterone system (RAAS) on sodium?
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Which equation represents the relationship between sodium excreted, filtered, and reabsorbed?
Which equation represents the relationship between sodium excreted, filtered, and reabsorbed?
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What percentage of potassium (K) is found in the extracellular fluid (ECF)?
What percentage of potassium (K) is found in the extracellular fluid (ECF)?
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Which of the following accurately describes the effect of hyperkalemia and hypokalemia on cardiac function?
Which of the following accurately describes the effect of hyperkalemia and hypokalemia on cardiac function?
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In which part of the nephron is potassium actively reabsorbed?
In which part of the nephron is potassium actively reabsorbed?
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How is most potassium found in urine derived?
How is most potassium found in urine derived?
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What happens to potassium secretion during potassium depletion?
What happens to potassium secretion during potassium depletion?
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What is the primary factor that alters the rate of potassium secretion?
What is the primary factor that alters the rate of potassium secretion?
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What triggers the adrenal cortex to increase aldosterone output?
What triggers the adrenal cortex to increase aldosterone output?
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What is the role of aldosterone in potassium regulation?
What is the role of aldosterone in potassium regulation?
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What is the primary role of aldosterone in the kidneys?
What is the primary role of aldosterone in the kidneys?
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What is a potential effect of aldosterone deficiency in hypoadrenocorticism?
What is a potential effect of aldosterone deficiency in hypoadrenocorticism?
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Which of the following conditions is associated with insufficient aldosterone secretion?
Which of the following conditions is associated with insufficient aldosterone secretion?
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What is the mechanism by which spironolactone functions as a diuretic?
What is the mechanism by which spironolactone functions as a diuretic?
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In which cell type of the collecting ducts does aldosterone primarily stimulate sodium reabsorption?
In which cell type of the collecting ducts does aldosterone primarily stimulate sodium reabsorption?
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What condition may arise if aldosterone secretion leads to excessive sodium retention?
What condition may arise if aldosterone secretion leads to excessive sodium retention?
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Which of the following symptoms is NOT typically associated with hypothalamic-hypoadrenocorticism?
Which of the following symptoms is NOT typically associated with hypothalamic-hypoadrenocorticism?
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How does the body respond to a decline in plasma potassium concentration related to aldosterone?
How does the body respond to a decline in plasma potassium concentration related to aldosterone?
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What is the primary role of the sodium-potassium ATPase pump in the basolateral cell membrane?
What is the primary role of the sodium-potassium ATPase pump in the basolateral cell membrane?
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What mechanism allows the sodium-chloride co-transporter to function effectively?
What mechanism allows the sodium-chloride co-transporter to function effectively?
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What happens to chloride ions after they enter the cell through the sodium-chloride co-transporter?
What happens to chloride ions after they enter the cell through the sodium-chloride co-transporter?
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What triggers the granular cells to secrete more renin?
What triggers the granular cells to secrete more renin?
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Which statement accurately describes the role of aldosterone in sodium reabsorption?
Which statement accurately describes the role of aldosterone in sodium reabsorption?
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How does a high intracellular potassium concentration affect potassium ion movement?
How does a high intracellular potassium concentration affect potassium ion movement?
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What role does increased sympathetic activity play in renin secretion?
What role does increased sympathetic activity play in renin secretion?
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What is the function of K leak channels in the distal and collecting tubules?
What is the function of K leak channels in the distal and collecting tubules?
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Study Notes
Renal Physiology Lectures 5-7
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Tubular Reabsorption Objectives:
- Explain sodium reabsorption and the function of Na/K ATPase.
- Describe the mechanism of water, urea, and chloride reabsorption in the proximal tubule.
- Explain the reabsorption of peptides and small molecular weight proteins in the proximal tubules.
- Clinical correlation-Proteinuria.
Trans-epithelial Transport
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Substances must cross five barriers to be reabsorbed from filtrate to plasma:
- Luminal cell membrane
- Cytosol
- Basolateral cell membrane
- Interstitial fluid
- Capillary wall
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Steps of Trans-epithelial Transport:
- Step 1: Substance leaves tubular fluid by crossing the luminal membrane.
- Step 2: Substance passes through the cytosol from one side of the tubular cell to another.
- Step 3: Substance crosses the basolateral membrane to enter the interstitial fluid.
- Step 4: Substance diffuses through the interstitial fluid.
- Step 5: Substance diffuses through the capillary wall to enter the blood.
Sodium Reabsorption by Various Nephron Parts
- 65% of sodium is reabsorbed in the proximal tubule, 25% in the loop of Henle, and 4-8% in the distal and collecting tubule.
- Proximal tubule reabsorption is crucial for glucose, amino acids, water, chloride, and urea.
- Loop of Henle reabsorption plays a role in producing urine with varying concentrations.
- Distal and collecting tubule reabsorption is variable and controlled by hormones, crucial for regulating ECF volume and arterial blood.
Active Na-K ATPase Pump
- 80% of the kidney's energy is spent running the Na-K ATPase pump.
- The pump actively extrudes Na from the cell, building up Na concentration in the lateral space.
- This creates a concentration gradient that facilitates passive Na movement from the tubular lumen into the tubular cell.
- Sodium continues to diffuse down a concentration gradient from the lateral space to the interstitial fluid.
Active Na Reabsorption Responsible for Passive Reabsorption
- Water is passively reabsorbed throughout the tubule, following Na.
- Approximately 65-117 liters of filtered water per day is passively reabsorbed by the end of the proximal tubule.
- Reabsorption primarily occurs via aquaporin 1 water channels.
- The return of filtered water to plasma is enhanced by higher osmotic pressure in peritubular capillaries.
Active Na Reabsorption for Urea Reabsorption
- Urea reabsorption at the glomerulus is identical to its concentration in the entering peritubular capillaries.
- Osmotically induced water reabsorption, secondary to active Na reabsorption, creates a concentration gradient for passive urea reabsorption.
- Only approximately 50% of filtered urea is passively reabsorbed.
Reabsorption of Filtered Peptides by the Proximal Tubule
- Substances with approximately 10 kDa are freely filtered at the glomerulus.
- Molecular weight increases cause a decline in filtered solute amounts.
- The proximal tubule actively reabsorbs filtered peptides and low-molecular-weight proteins.
- Proteins are broken down into amino acids and reabsorbed via co-transport with Na.
Reabsorption of Low Molecular Weight Proteins
- Low-molecular-weight filtered proteins (insulin, glucagon, parathyroid hormone) are absorbed via receptor-mediated endocytosis.
- These proteins bind to receptors (megalin, cubilin) in the plasma membrane, leading to endocytosis.
- Endocytosed proteins are delivered to lysosomes for degradation and recycling.
Clinical Correlation: Proteinuria
- Proteinuria can be categorized as normal, overflow, glomerular, or tubular.
Objectives for Renal Physiology
- Glucose reabsorption in the proximal tubule.
- Sodium and potassium handling in the loop of Henle, distal convoluted tubules, and collecting tubules.
- Mechanism of action of aldosterone.
- Potassium handling in different parts of the nephron.
- Aldosterone-clinical correlation (Hypoadrenocorticism).
- Aldosterone antagonists as diuretics.
Glucose Reabsorption in Proximal Tubules
- Glucose is reabsorbed via Na-dependent secondary active transport.
- Sodium and glucose are simultaneously transported into the cell by SGLT.
- A limited number of SGLT molecules limits the maximum amount of glucose that can be actively transported.
Mechanisms of Sodium, Chloride, and Potassium Transport in the Thick Ascending Loop of Henle
- The sodium-potassium ATPase pump maintains low intracellular sodium concentration.
- The 1-sodium, 2-chloride, 1-potassium co-transporter moves these ions from the tubular lumen into the cells.
- Energy from sodium diffusion creates the driving force for transport.
Mechanism of Sodium Chloride Transport in the Early Distal Tubule
- The sodium-potassium ATPase pump in the basolateral membrane maintains low intracellular sodium concentration.
- The sodium-chloride co-transporter moves sodium and chloride from the tubular lumen into the cells.
- Chloride diffuses out of the cell through chloride channels in the basolateral membrane and into the renal interstitial fluid.
Diuretics
- Various diuretics (loop, thiazide, K+-sparing, carbonic anhydrase inhibitors) have different mechanisms of action that influence sodium and water reabsorption in the kidney.
Activation of the Renin-Angiotensin-Aldosterone System
- Granular cells function as intrarenal baroreceptors.
- Decreased NaCl triggers macula densa cells to stimulate renin secretion.
- Increased sympathetic activity also stimulates renin secretion.
Regulation of Na Reabsorption and Potassium Ion Secretion
- Na/K ATPase pump moves Na out of the cell and transports K from the lateral space into the principal cells of CT. This process enables high intracellular K concentration, facilitating passive K movement into the tubular lumen via leak channels.
- K is then moved out of the peritubular capillary plasma into the interstitial fluid.
Mechanism of Action of Aldosterone
- Acute Effects: Promotes Na+ reabsorption and K+ secretion via stimulating Na+/K+-ATPase activity and increasing open probability of Na+ channels (ENaC).
- Chronic Effects: Increases Na+/K+-ATPase abundance, expression of NaCl co-transporter (NCC) in the distal convoluted tubule and ENaC in collecting duct principal cells.
Summary of Na Handling by the Kidney
- Kidneys adjust salt excretion by regulating GFR and Na reabsorption.
- Na reabsorption in the distal and collecting tubules is a function of the renin-angiotensin-aldosterone system.
- The RAAS promotes Na retention by stimulating Na reabsorption. Amount of filtered Na is controlled by GFR and amount of salt excreted by two processes.
Distribution of Potassium in Body Compartments
- Potassium is primarily intracellular (98%), with small amounts in the extracellular fluid.
- Small changes in extracellular K concentrations can significantly impact the body's membrane electrical activity (excitable tissues).
Potassium Handling by the Kidney
- Potassium is actively reabsorbed in the proximal tubule and loop of Henle, and primarily secreted in the distal and collecting tubules.
- Potassium secretion is controlled by the principal cells and other cells.
- Potassium secretion in distal parts is important to maintaining a balance of K concentrations in the body.
Regulation of Potassium Secretion
- Several factors alter the rate of K secretion, with aldosterone being the most influential.
- Elevation in systemic potassium stimulates the adrenal cortex to release more aldosterone. Increased aldosterone causes increased K secretion and Na reabsorption.
Aldosterone Functions in the Kidney
- Aldosterone affects principal cells of the collecting ducts by increasing Na reabsorption and promoting K secretion.
- Aldosterone stimulates hydrogen secretion in intercalated cells of the collecting ducts. Both of these processes contribute to electrolyte and acid-base balance.
Hypoadrenocorticism (Addison's Disease)
- Aldosterone deficiency is a key characteristic.
- Other symptoms include hyperkalemia, hyponatremia, hypochloremia and metabolic acidosis, polyuria, polydipsia, weakness, recurrent vomiting, and diarrhea.
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Description
Dive deep into the mechanisms of tubular reabsorption and trans-epithelial transport in the kidneys. Learn how sodium, water, urea, and proteins are reabsorbed, alongside the critical role of Na/K ATPase. This quiz also addresses clinical implications, particularly proteinuria, enhancing your understanding of renal function.