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Renal Autoregulation of GFR:


___ is so named because part of the renal tubules—the macula densa of the juxtaglomerular apparatus—provides feedback to the glomerulus (Figure 24.10). When GFR is above normal due to elevated systemic blood pressure, filtered fluid flows more rapidly along the renal tubules. As a result, the proximal convoluted tubule and nephron loop have less time to reabsorb Na+, Cl−, and water. Macula densa cells are thought to detect the increased delivery of Na+, Cl−, and water in the filtered fluid and respond by inhibiting nitric oxide (NO) release from cells in the juxtaglomerular apparatus. When NO is released, it stimulates afferent arterioles to dilate; when NO release is inhibited, afferent arterioles constrict, resulting in decreased blood flow into the glomerular capillaries, and decreased GFR. On the other hand, as blood pressure falls (resulting in decreased GFR), filtered fluid flows more slowly along the renal tubules (allowing time for reabsorption), and the release of NO from the juxtaglomerular apparatus is no longer inhibited by the macula densa cells. As the level of NO increases, afferent arterioles dilate, increasing blood flow into the glomerulus, and increasing GFR. Macula densa cells also inhibit release of renin from juxtaglomerular cells when increased Na+ and Cl− is detected in filtered fluid. As you will see in Concept 24.7, this links renal autoregulation of GFR with hormonal regulation of tubular reabsorption and secretion.
An increase in blood volume, as might occur after you finish a supersized drink, stretches the atria of the heart and promotes release of atrial natriuretic peptide. Atrial natriuretic peptide increases natriuresis, the urinary loss of Na+. As Na+ is excreted, followed by Cl− and water, blood volume decreases. An increase in blood volume also slows release of renin from kidney juxtaglomerular cells. When renin level drops, less angiotensin II is formed. Decline in angiotensin II increases glomerular filtration rate and reduces Na+, Cl−, and water reabsorption in the kidney tubules. In addition, less angiotensin II leads to less aldosterone, which decreases Na+ and Cl− reabsorption in the collecting ducts. As more Na+ and Cl− ions are excreted in the urine, more water is lost in urine, which decreases blood volume. By contrast, when someone becomes dehydrated, higher levels of angiotensin II and aldosterone promote urinary reabsorption of Na+ and Cl−, and water by osmosis with the solutes, and thereby conserve the volume of body fluids.
The major hormone that regulates water loss is antidiuretic hormone (ADH). An increase in the osmotic pressure of body fluids not only stimulates the thirst mechanism, as previously discussed, but also stimulates release of ADH (see Figure 24.17). ADH promotes water reabsorption by the collecting ducts. As a result, water is reabsorbed from the tubular fluid and a small volume of concentrated urine is produced. By contrast, intake of water decreases the osmotic pressure of body fluids. Within minutes, ADH secretion shuts down, collecting ducts become less permeable to water, and more water is lost in the urine.