Renal System 3: Regulation

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Autoregulation (at the local level)

Autoregulation maintains the glomerular filtration rate despite changes in local blood pressure and blood flow. It does this by altering the diameters (lumen width) of the afferent and efferent arterioles, as well as the glomerular capillaries. The arterioles are changed through a myogenic mechanism, whereas tubuloglomerular feedback is responsible for changes in the glomerulus.

The myogenic mechanism involves stretch receptors:
  • ↑ blood pressure → afferent arteriole wall stretches, smooth muscle contrasts, afferent arterioles constrict, ↓ glomerular blood flow and pressure → ↓ net filtration pressure → ↓ glomerular filtration rate (see 1)
  • ↓ blood pressure → dilation of afferent arteriole and glomerular capillaries, constriction of efferent arteriole, ↑ glomerular blood pressure → ↑ net filtration pressure → ↑ glomerular filtration rate (see 2)
The tubuloglomerular feedback mechanism involves paracrine factors (local hormones):
  1. GFR increases to an abnormal level
  2. Flow through the tubule increases
  3. Flow past macula densa cells of the distal convoluted tubule increases (passes between afferent and efferent arterioles)
  4. Paracrine signal from the macula densa is sent to the afferent arteriole
  5. Afferent arteriole smooth muscle constricts, increasing resistance (see 1)
  6. The hydrostatic pressure in the glomerulus decreases
  7. GFR decreases to a homeostatic level

Autonomic Regulation

The glomerular filtration rate is regulated by the sympathetic nervous system: 

↑ sympathetic activity → vasoconstriction of afferent arterioles (see 1)

Hormonal Regulation

There are two hormonal mechanisms by which glomerular filtration rate is regulated.

     1.   Renin-Angiotensin System

This system developed its name from the fact that a release of renin activates angiotensin to change its configuration, which is then further changed by an enzyme to become a functional version of angiotensin.

Renin is released from the juxtaglomerular complex due to three stimuli:
  • Decreased blood volume detected by baroreceptors in the afferent arteriole
  • Stimulation of granular cells by the renal sympathetic nerves
  • Decreased osmotic concentration of the tubular fluid detected by the macula densa of the DCT
Once renin is released, it converts angiotensin (with no function) to angiotensin 1, which still has no function. Angiotensin converting enzyme (ACE) then converts angiotensin 1 to angiotensin 2, which has several functions summarised below:
  • Increases sympathetic motor tone: constriction of venous reservoirs, increases cardiac output, stimulates peripheral vasoconstriction
  • Constricts efferent arterioles of the nephron: ↑ GFR and ↑ NFP
  • Stimulates reabsorption of sodium ions and water at the proximal convoluted tubule
  • Stimulates secretion of aldosterone from the adrenal cortex: ↑ Na+ reabsorption in the distal convoluted tubule and collecting ducts
  • Stimulates thirst
  • Triggers the release of anti-diuretic hormone (ADH) from the hypothalamus: ↑ water reabsorption in distal convoluted tubule and collecting ducts, prevents diuresis
     2.   Natriuretic Peptides (ANP and BNP)

Natriuretic peptides are released by the heart in response to very large increases in blood volume or pressure, which is the opposite stimulus to the renin-angiotensin system. Stretch receptors in the heart wall trigger the release of ANP from atria and BNP from the ventricles. Natriuretic peptides override other mechanisms and have an extremely rapid effect, unlike the slower hormonal response of the renin-angiotensin system.

ANP and BNP trigger dilation of afferent arterioles and constriction of efferent arterioles, elevating the glomerular pressures and thus its filtration rate. This overall increases urine production.

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