Regulation of GFR: autoregulation via myogenic mechanism Myogenic mechanism

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• GFR can be regulated by adjusting: • Blood flow in and out of the glomerular capillaries. • Surface area of glomerular capillaries. • There are three main ways to make these adjustments: • Renal autoregulation. • Nervous regulation. • Renal autoregulation occurs when the kidneys themselves regulate blood flow. • Two renal autoregulatory mechanisms maintain normal GFR over a wide range of systemic blood pressures. • As systemic blood pressure goes up, the smooth muscle cells in the afferent arterioles stretch. • The smooth muscle fibers of the afferent arterioles respond to stretching by contracting, reducing blood flow to the glomerular capillaries. • GFR decreases. • As systemic blood pressure goes down, the smooth muscle cells in the afferent arteriole relax. • The relaxation of the afferent arteriole allows greater blood flow to the capillaries. • GFR increases. Autoregulation via tubuloglomerular feedback Tubuloglornerular feedback. • When blood pressure is above normal, rapid filtrate flow reduces ion retention so filtrate in tubule has more Na+, Cl-, 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. Neural regulation • 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 OFR. • This mechanism eventually reduces urine output, conserving water. Hormonal regulation • 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 11. • 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.

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