Urine Formation

    Cards (21)

    • Urine Formation
      The process by which the kidneys produce urine
    • An adult man can produce around 2L of urine per day
    • Urine Formation
      1. Glomerular filtration
      2. Tubular reabsorption
      3. Tubular secretion
    • Glomerular filtration
      A passive process where water and most solutes in blood plasma filter across the wall of glomerular capillaries into the glomerular capsule and then into the renal tubule
    • The daily volume of glomerular filtrate in adults is 150 liters in females and 180 liters in males
    • More than 99% of the glomerular filtrate returns to the blood stream via tubular reabsorption, so only 1–2 liters (about 1%) is excreted as urine
    • Glomerulus
      • It is a very efficient filter because its filtration membrane is porous and very permeable, it has a large surface area, and glomerular blood pressure is higher (55 mm Hg) than other capillaries
      • Molecules >5 nm are not filtered (e.g., plasma proteins) and function to maintain colloid osmotic pressure of the blood
    • Glomerular filtrate
      The fluid that enters the capsular space after filtration
    • The glomerular filtrate differs from the plasma by lacking proteins and large molecules
    • Glomerular filtration depends on three main pressures
      1. Glomerular blood hydrostatic pressure (promotes filtration)
      2. Capsular hydrostatic pressure (opposes filtration)
      3. Blood colloid osmotic pressure (opposes filtration)
    • Net filtration pressure (NFP)
      The total pressure that promotes filtration, determined as GBHP - CHP - BCOP
    • Glomerular filtration rate (GFR)

      The amount of filtrate formed in all renal corpuscles of both kidneys each minute
    • In adults, the GFR averages 125 mL/min in males and 105 mL/min in females
    • Homeostasis of body fluids requires that the kidneys maintain a relatively constant GFR
      1. Renal auto-regulation of GFR
      2. Neural regulation of GFR
      3. Hormonal regulation of GFR
    • Renal auto-regulation of GFR - Myogenic mechanism

      1. As BP rises, GFR also rises because renal blood flow increases
      2. The elevated BP stretches the walls of the afferent arterioles
      3. Smooth muscle fibers in the wall of the afferent arteriole contract, which narrows the arteriole's lumen
      4. Renal blood flow decreases, reducing GFR
      5. When arterial BP drops, the smooth muscle cells relax, the afferent arterioles dilate, renal blood flow increases, and GFR increases
    • Renal auto-regulation of GFR - Tubuloglomerular feedback
      1. When GFR is increased, filtered fluid flows more rapidly along the renal tubules
      2. Macula densa cells sense the increased delivery of Na+, Cl-, and water and inhibit release of nitric oxide (NO) from cells in the juxtaglomerular apparatus (JGA)
      3. Afferent arterioles constrict when the level of NO declines, thus glomerular blood flow and GFR decreases
      4. When GFR is decreased, the opposite sequence of events occurs
    • Neural regulation of GFR
      1. Norepinephrine causes vasoconstriction of the renal arterioles
      2. During a stressful event, vasoconstriction of the afferent arterioles predominates, glomerular blood flow and GFR greatly decrease
    • Hormonal regulation of GFR
      1. Angiotensin II narrows both afferent and efferent arterioles and reduces renal blood flow, thereby decreasing GFR
      2. Atrial natriuretic peptide (ANP) increases the GFR
    • Homeostatic regulation of tubular reabsorption and tubular secretion
      Angiotensin II, Aldosterone, Antidiuretic hormone, Atrial natriuretic peptide, and Parathyroid hormone affect the extent of Na+, Cl-, Ca+2 and water reabsorption as well as K+ secretion by the renal tubules
    • Atrial natriuretic peptide (ANP)
      It increases the excretion of Na+ in urine (natriuresis) and increases urine output (diuresis), which decreases blood volume and blood pressure
    • Parathyroid hormone (PTH)
      It stimulates the renal tubular cells to reabsorb more Ca+2 into the blood while inhibits HPO4-2 (phosphate) reabsorption thereby promoting phosphate excretion