The distal tubule and collecting duct experience a decrease in Na+ reabsorption when there is ECFV expansion. The amount of Na+ delivered to the distal tubule is greater than that in a euvolemic state, proportional to the degree of ECFV expansion. The increased Na+ load overwhelms the reabsorptive capacity of the distal tubule and collecting duct, which is further impaired by reduced levels of angiotensin II and aldosterone, as well as increased levels of natriuretic peptides. As a result, there is an increased excretion of water. This leads to a decrease in plasma osmolality, reducing the secretion of AVP. Elevated levels of natriuretic peptides also contribute to the decrease in AVP secretion. Natriuretic peptides also inhibit the action of AVP on the collecting duct, leading to a decrease in water reabsorption and an increase in water excretion by the kidneys. Therefore, the excretion of NaCl and water occurs together, restoring euvolemia and maintaining constant body fluid osmolality. The time it takes for this response to occur depends on the magnitude of ECFV expansion, ranging from hours to days. If the ECFV expansion is small, euvolemia is generally restored within 24 hours. However, with larger degrees of ECFV expansion, it can take several days for the response to occur.

In summary, the renal response to ECFV expansion involves the integrated action of all parts of the nephron. Firstly, the amount of filtered Na+ increases. Secondly, Na+ reabsorption by the proximal tubule and loop of Henle is reduced, and glomerulotubular balance does not occur in this condition. Lastly, reabsorption of Na+ by the distal tubule and collecting duct is decreased, while the delivery of Na+ is increased, primarily due to a reduction in aldosterone. This results in the excretion of a larger fraction of the filtered Na+, thereby restoring euvolemia.

During ECFV contraction, signals from the high-pressure and low-pressure vascular volume sensors prompt the kidneys to reduce NaCl and water excretion, restoring ECFV. These signals include increased renin secretion, leading to elevated levels of angiotensin II and increased secretion of aldosterone by the adrenal cortex. Additionally, the secretion of ANP, BNP, and urodilatin is inhibited, while AVP secretion is stimulated by the posterior pituitary. The integrated response of the nephron to these signals is illustrated in Figure 35.13. The general response includes a decrease in GFR, caused by constriction of the afferent and efferent arterioles due to increased renal sympathetic nerve activity. This results in a greater effect on the afferent arteriole, leading to a decrease in hydrostatic pressure in the glomerular capillaries and a subsequent decrease in GFR. The decrease in GFR reduces the filtered amount of Na+.
3. Na+ reabsorption decreases in the distal tubule and collecting duct. As noted, the amount of Na+ delivered to the distal tubule exceeds that observed in the euvolemic state (i.e., the amount of Na+ delivered to the distal tubule varies in proportion to the degree of ECFV expansion). This increased load of Na+ overwhelms the reabsorptive capacity of the distal tubule and the collecting duct, and this capacity is also impaired by reduced levels of angiotensin II and aldosterone, as well as increased levels of natriuretic peptides. The final component in the response to ECFV expansion is increased excretion of water. As Na+ excretion increases, plasma osmolality begins to fall. This decreases secretion of AVP. AVP secretion is also decreased in response to the elevated levels of natriuretic peptides. In addition, natriuretic peptides inhibit the action of AVP on the collecting duct. Together, these effects decrease water reabsorption by the collecting duct and thereby increase water excretion by the kidneys. Thus excretion of NaCl and water occurs in concert; euvolemia is restored and body fluid osmolality remains constant. The time course of this response (hours to days) depends on the magnitude of the ECFV expansion. Thus if the degree of ECFV expansion is small, the mechanisms just described generally restore euvolemia within 24 hours. However, with large degrees of ECFV expansion, the response can take several days.
In brief, the renal response to ECFV expansion involves the integrated action of all parts of the nephron; (1) the amount of Na+ filtered is increased, (2) Na+ reabsorption by the proximal tubule and loop of Henle is reduced (glomerulotubular balance does not occur under this condition), and (3) reabsorption of Na+ by the distal tubule and collecting duct is decreased (while the delivery of Na+ is increased), primarily secondary to a reduction in aldosterone. In summary, ECFV expansion leads to a reduction in Na+ reabsorption by both the proximal tubule and the ASDN, which results in excretion of a larger fraction of the filtered Na+ , thereby restoring euvolemia.
Control of NaCl Excretion With Volume Contraction
During ECFV contraction, the high-pressure and low-pressure vascular volume sensors send signals to the kidneys to reduce NaCl and water excretion and thereby restore ECFV. The signals that act on the kidneys include: 1.
2.
increased secretion of renin, which results in elevated angiotensin II levels and thus increased secretion of aldosterone by the adrenal cortex 3.
inhibition of ANP and BNP secretion by the heart and urodilatin production by the kidneys 4.
stimulation of AVP secretion by the posterior pituitary
The integrated response of the nephron to these signals is illustrated in
Fig. 35.13 . The general response is as follows (the numbers correlate with those encircled in
Fig. 35.13): 1.
GFR decreases. Afferent and efferent arteriolar constriction occurs as a result of increased renal sympathetic nerve activity. The effect appears to be greater on the afferent than on the efferent arteriole, because the hydrostatic pressure in the glomerular capillaries fall, which thereby decreases GFR. Because RPF decreases more than GFR, filtration fraction increases. The decrease in GFR reduces the filtered amount of Na+ .
2.