Regulation of GFR: autoregulation via tubuloglomerular feedback, neural & hormonal regulation

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• When blood pressure is above normal, rapid filtrate flow reduces ion retention so filtrate in tubule has more Na+, C1-, and water.
• It is believed that vasoconstricting chemicals from the juxtaglomerular cells are released when the macula densa cells detect higher water and ion levels in the tubule.
• These chemicals cause vasoconstriction of the afferent arteriole, thereby reducing blood flow to the glomerular capillaries.
• GFR decreases.
• Slow filtrate flow increases ion retention so filtrate in the tubule has less Na+, Cl-, and water.
• Macula densa cells detect lower water and ion levels in the tubules, inhibiting the release of vasoconstricting chemicals from the juxtaglomerular cells.
• The afferent arteriole vasodilates, increasing blood flow to the glomerular capillaries.
• GFR increases.

• At rest, sympathetic stimulation is weak and renal autoregulation is the dominant mechanism for controlling GFR.
• Sympathetic stimulation is most important during extreme rises or falls in blood pressure.
• In the case of an extreme drop in blood pressure, sympathetic output increases.
• The afferent arterioles vasoconstrict.
• The juxtaglomerular cells secrete renin, a chemical that promotes formation of angiotensin II, a potent vasoconstrictor.
• The net result of increased sympathetic stimulation is a reduction of blood flow to the glomerular capillaries - a decrease of GFR.
• This mechanism eventually reduces urine output, conserving water.

• If both blood volume and pressure drop, the walls of the renal arterioles collapse. This causes the juxtaglomerular cells to produce renin.
• Renin promotes the formation of angiotensin H.
• Increased angiotensin II promotes vasoconstriction of afferent arterioles, reducing blood flow to the glomerular capillaries.
• GFR decreases.
• A sudden large increase in blood pressure will cause the atria of the heart to stretch.
• ANP is released into the bloodstream.
• ANP causes the mesangial cells of the glomerulus to relax, increasing the surface area of the capillaries.
• Increased filtering area increases OFR.
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I believe the vasoconstriction of the afferent arterioles via angiotensin II depends on how much angiotensin II is released. I am still GFR regulation but I do believe it depends on how much angiotensin II is released because of the efferent areteriole being more sensitive to angiotensin II than the afferent arteriole. Again, I am still so very confused about the intrinsic and extrinsic controls of GFR.

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