Relative amounts of (a) glomerular filtrate and (b) urine formed in twenty-four hours.
The hydrostatic pressure in the glomerular capsule is another factor that may affect net filtration pressure and rate. This capsular pressure sometimes changes as a result of an obstruction, such as a stone in a ureter or an enlarged prostate gland pressing on the urethra. If this occurs, fluids back up into the renal tubules and raise the hydrostatic pressure in the glomerular capsules. Because any increase in capsular pressure opposes glomerular filtration, filtration rate may decrease significantly.
At rest, the kidneys receive approximately 25% of the cardiac output, and about 20% of the blood plasma is filtered as it flows through the glomerular capillaries. This means that in an average adult, the glomerular filtration rate for the nephrons of both kidneys is about 125 milliliters per minute, or 180,000 milliliters (180 liters) in twenty-four hours. Assuming that the blood plasma volume is about 3 liters, the production of 180 liters of filtrate in twenty-four hours means that all of the plasma must be filtered through the glomeruli about sixty times each day (fig. 20.17). Since this twenty-four-hour volume is nearly 45 gallons, it is obvious that not all of it is excreted as urine. Instead, most of the fluid that passes through the renal tubules is reabsorbed and reenters the plasma.
The volume of plasma the kidneys filter also depends on the surface area of the glomerular capillaries. This surface area is estimated to be about 2 square meters— approximately equal to the surface area of an adult's skin.
An injury to a kidney can be more dangerous than an injury to another organ. An injured kidney produces a protein called transforming growth factor beta, which causes scars to form. The scars further damage the kidney, impairing its function.
U What processes occur in urine formation?
^9 How is filtration pressure calculated?
^9 What factors influence the rate of glomerular filtration?
In general, glomerular filtration rate remains relatively constant through a process called autoregulation. However, certain conditions override autoregulation. GFR may increase, for example, when body fluids are in excess and decrease when the body must conserve fluid.
Recall from chapter 11 (p. 442) that sympathetic nervous system fibers synapse with the vascular smooth muscle of arterioles. Reflexes responding to changes in blood pressure and volume control the activity of these sympathetic fibers. If blood pressure and volume drop, vasoconstriction of the afferent arterioles results, decreasing filtration pressure and thus GFR. The result is an appropriate decrease in the rate of urine formation when the body must conserve water. If receptors detect excess body fluids, vasodilation of the afferent arteriole results, increasing filtration pressure and GFR.
A second control of GFR is the hormonelike renin-angiotensin system. The juxtaglomerular cells of the afferent arterioles secrete an enzyme, renin, in response to stimulation from sympathetic nerves and pressure-sensitive cells called renal baroreceptors that are in the afferent arteriole. These factors stimulate renin secretion if blood pressure drops. The macula densa also controls renin secretion. Cells of the macula densa sense the concentrations of sodium, potassium, and chloride ions in the distal renal tubule. Decreasing levels of these ions stimulate renin secretion.
Once in the bloodstream, renin reacts with the plasma protein angiotensinogen to form angiotensin I. An enzyme, angiotensin-converting enzyme (ACE), present on capillary endothelial cells (particularly in the lungs), rapidly converts angiotensin I to angiotensin II.
Angiotensin II has a number of renal effects that help maintain sodium balance, water balance, and blood pressure (fig. 20.18). As a vasoconstrictor, it affects both
- Increased aldosterone secretion
• Increased ADH secretion Increased thirst
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