The net filtration pressure that drives fluids from glomerular capillaries into the capsule lumen of Bowman’s capsule has three components. The first two are the same as in any capillary bed: local blood pressure driving fluids out and oncotic pressure keeping fluids in. The third component is peculiar to glomerular filtration and is due to the fact that the fluids are pumped into a capsule that exerts a back-pressure opposing flow.
Formally, the components of net filtration pressure (NFP) are GHP, the glomerular hydrostatic pressure (local blood pressure); BCOP, blood colloid osmotic pressure (oncotic pressure due to proteins in blood) which draws water into the plasma; and, CHP, capsular hydrostatic pressure (pressure in the enclosed space of the capsule). Typically, NFP = GFP – BCOP – CHP = 55 – 30 – 15 = 10 mm Hg, a relatively small pressure. As a result of this low pressure, the filtration fraction (the fraction of blood entering the glomerulus that is filtered) is about 20%. The rest passes out the efferent arteriole.
Autoregulation of the GFR is primarily a local control. The macula densa cells at the junction of ascending limb of loop of Henle and DCT (near afferent arteriole) respond to changes in the NaCl concentration of the tubule fluids. Increased systemic BP increases urine flow rate in the loop of Henle, causing less NaCl reabsorption in the ascending limb. Macula densa cells respond to the increased NaCl by secreting a paracrine vasopressor that acts on the afferent arterioles. When the afferent arterioles vasoconstrict, renal blood flow is reduced. The result is a decrease in glomerular hydrostatic pressure and a return of GFR to its normal value, in spite of the increase in systemic BP.
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