Afferent arteriolar end
Efferent! arteriolar end
^FffifflRBESin^ Pressure profiles along a skeletal muscle capillary and a glomerular capillary. A, In the typical skeletal muscle capillary, filtration occurs at the arterial end and absorption at the venous end of the capillary. Interstitial fluid hydrostatic and colloid osmotic pressures are neglected here because they are about equal and counterbalance each other. B, In the glomerular capillary, glomerular hydrostatic pressure (Pgc) (top line) is high and declines only slightly with distance. The bottom line represents the hydrostatic pressure in
Bowman's capsule (PBS). The middle line is the sum of PBS and the glomerular capillary colloid osmotic pressure (COP). The difference between PGC and PBS + COP is equal to the net ultrafiltration pressure gradient (UP). In the normal human glomerulus, filtration probably occurs along the entire capillary. Assuming that Kf is uniform along the length of the capillary, filtration rate would be highest at the afferent arteriolar end and lowest at the efferent arteriolar end of the glomerulus.
man's capsule, and the glomerular capillary colloid osmotic pressure. These factors are discussed next.
The Glomerular Ultrafiltration Coefficient. The glomerular ultrafiltration coefficient (Kf) is the glomerular equivalent of the capillary filtration coefficient encountered in Chapter 16. It depends on both the hydraulic conductivity (fluid permeability) and surface area of the glomerular filtration barrier. In chronic renal disease, functioning glomeruli are lost, leading to a reduction in surface area available for filtration and a fall in GFR. Acutely, a variety of drugs and hormones appear to change glomerular Kf and, thus, alter GFR, but the mechanisms are not completely understood.
Glomerular Capillary Hydrostatic Pressure. Glomerular capillary hydrostatic pressure (PGC) is the driving force for filtration; it depends on the arterial blood pressure and the resistances of upstream and downstream blood vessels. Because of autoregulation, PGC and GFR are maintained at relatively constant values when arterial blood pressure is varied from 80 to 180 mm Hg. Below a pressure of 80 mm Hg, however, PGC and GFR decrease, and GFR ceases at a blood pressure of about 40 to 50 mm Hg. One of the classic signs of hemorrhagic or cardiogenic shock is an absence of urine output, which is due to an inadequate PGC and GFR.
The caliber of afferent and efferent arterioles can be altered by a variety of hormones and by sympathetic nerve stimulation, leading to changes in PGC, glomerular blood flow, and GFR. Some hormones act preferentially on afferent or efferent arterioles. Afferent arteriolar dilation increases glomerular blood flow and PGC and, therefore, produces an increase in GFR. Afferent arteriolar constriction produces the exact opposite effects. Efferent arteriolar dilation increases glomerular blood flow but leads to a fall in GFR because PGC is decreased. Constriction of efferent arterioles increases PGC and decreases glomerular blood flow. With modest efferent arteriolar constriction, GFR increases because of the increased PGC. With extreme efferent arteriolar constriction, however, GFR decreases because of the marked decrease in glomerular blood flow.
Hydrostatic Pressure in Bowman's Capsule. Hydrostatic pressure in Bowman's capsule (Pbs) depends on the input of glomerular filtrate and the rate of removal of this fluid by the tubule. This pressure opposes filtration. It also provides the driving force for fluid movement down the tubule lumen. If there is obstruction anywhere along the urinary tract—for example, stones, ureteral obstruction, or prostate enlargement—then pressure upstream to the block is increased, and GFR consequently falls. If tubular reabsorption of water is inhibited, pressure in the tubular system is increased because an increased pressure head is needed to force a large volume flow through the loops of Henle and collecting ducts. Consequently, a large increase in urine output caused by a diuretic drug may be associated with a tendency for GFR to fall.
COP opposes glomerular filtration. Dilution of the plasma proteins (e.g., by intravenous infusion of a large volume of isotonic saline) lowers the plasma COP and leads to an increase in GFR. Part of the reason glomeru-lar blood flow has important effects on GFR is that the COP profile is changed along the length of a glomerular capillary. Consider, for example, what would happen if glomerular blood flow were low. Filtering a small volume out of the glomerular capillary would lead to a sharp rise in COP early along the length of the glomerulus. As a consequence, filtration would soon cease and GFR would be low. On the other hand, a high blood flow would allow a high rate of filtrate formation with a minimal rise in COP. In general, renal blood flow and GFR change hand in hand, but the exact relation between GFR and renal blood flow depends on the magnitude of the other factors that affect GFR.
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This ebook provides an introductory explanation of the workings of the human body, with an effort to draw connections between the body systems and explain their interdependencies. A framework for the book is homeostasis and how the body maintains balance within each system. This is intended as a first introduction to physiology for a college-level course.