The reabsorption of Na+ in the proximal tubule and loop of Henle is increased. Various mechanisms enhance Na+ reabsorption in the proximal tubule. For instance, increased levels of sympathetic nerve activity and angiotensin II directly stimulate Na+ reabsorption. The decrease in hydrostatic pressure within the glomerular capillaries also leads to a decrease in hydrostatic pressure within the peritubular capillaries. Additionally, the increased filtration fraction results in an increase in peritubular oncotic pressure. These changes in the capillary Starling forces promote fluid movement from the lateral intercellular space into the capillary, stimulating the reabsorption of NaCl and water in the proximal tubule. Increased sympathetic nerve activity, as well as elevated levels of angiotensin II and aldosterone, also stimulate Na+ reabsorption in the thick ascending limb.

Na+ reabsorption in the distal tubule and collecting duct is enhanced. The small amount of Na+ delivered to the ASDN, due to decreased filtration and increased reabsorption in the proximal tubule and loop of Henle, is almost entirely reabsorbed because transport in the segments of the ASDN is enhanced. The stimulation of Na+ reabsorption in the ASDN primarily occurs as a result of increased aldosterone levels, although increased sympathetic nerve activity and elevated levels of angiotensin II may also contribute to this response. Furthermore, the levels of natriuretic peptides, which inhibit collecting duct reabsorption, are reduced. Finally, AVP enhances water reabsorption in the latter portion of the distal tubule and the collecting duct. The levels of AVP are elevated through the activation of low and high-pressure vascular volume sensors, as well as by the elevated levels of angiotensin II. Consequently, water excretion is reduced. Since both water and Na+ are retained by the kidneys in equal proportions, euvolemia is restored and body fluid osmolality remains constant.

The restoration of ECFV (extracellular fluid volume) following ECFV contraction involves the integrated action of all segments of the nephron. The time frame and degree of attaining euvolemia depend on the magnitude of ECFV contraction and the dietary intake of Na+. If additional NaCl is consumed in the diet, euvolemia can be restored more rapidly.

To maintain regulation of body fluid osmolality, the amount of water added to the body must precisely match the amount lost from the body. Water loss occurs through various routes, such as respiration, sweating, and feces. The kidneys are the sole regulated route for water excretion. The excretion of water by the kidneys is controlled by AVP secreted from the posterior pituitary. When AVP levels are high, the kidneys excrete a small volume of hyperosmotic urine. When AVP levels are low, a large volume of hypoosmotic urine is excreted.
Na+ reabsorption by the proximal tubule and loop of Henle is increased. Several mechanisms augment Na+ reabsorption in the proximal tubule. For example, increased sympathetic nerve activity and angiotensin II levels directly stimulate Na+ reabsorption. The decreased hydrostatic pressure within the glomerular capillaries also leads to a decrease in the hydrostatic pressure within the peritubular capillaries. In addition, as just noted, the increased filtration fraction results in an increase in the peritubular oncotic pressure. These alterations in the capillary Starling forces facilitate movement of fluid from the lateral intercellular space into the capillary and thereby stimulate reabsorption of NaCl and water by the proximal tubule (see for a complete description of this mechanism). Increased sympathetic nerve activity as well as elevated levels of angiotensin II and aldosterone stimulate Na+ reabsorption by the thick ascending limb.
3.
Na+ reabsorption by the distal tubule and collecting duct is enhanced. The small amount of Na+ that is delivered to the ASDN, owing to decreased filtration and increased reabsorption by the proximal tubule and loop of Henle, is almost completely reabsorbed because transport in the segments of the ASDN is enhanced. Stimulation of Na+ reabsorption by the ASDN is primarily the result of increased aldosterone levels, although increased sympathetic nerve activity and increased angiotensin II levels may also contribute to this response. Lastly, levels of natriuretic peptides, which inhibit collecting duct reabsorption, are reduced. Finally, water reabsorption by the latter portion of the distal tubule and the collecting duct is enhanced by AVP, the levels of which are elevated through activation of the lowand high-pressure vascular volume sensors as well as by the elevated levels of angiotensin II. As a result, water excretion is reduced. Because both water and Na+ are retained by the kidneys in equal proportions, euvolemia is reestablished and ˜ AVP ° ANP and BNP Heart Brain ˜ Aldosterone Lung Adrenal gland ° Na+, H2O excretion ˜ Renin ˜ Sympathetic activity 2 1 3 ˜ Angiotensin I ˜ Angiotensin II Volume contraction • Fig. 35.13 Integrated response to ECFV contraction. Numbers refer to the description of the response in the text. ANP, atrial natriuretic peptide; BNP, brain natriuretic peptide; GFR, glomerular filtration rate; PNa+, plasma [Na+]; R, tubular reabsorption of Na+; UNa+V, Na+ excretion rate.
body fluid osmolality remains constant. The time course of this restoration of ECFV (hours to days) and the degree to which euvolemia is attained depend on the magnitude of ECFV contraction as well as the dietary intake of Na+ . Euvolemia can be restored more rapidly if additional NaCl is ingested in the diet.
In brief, the nephron’s response to ECFV contraction involves the integrated action of all its segments: (1) the 1.
Regulation of body fluid osmolality (i.e., steady-state balance) requires that the amount of water added to the body exactly matches the amount lost from the body. Water is lost from the body by several routes (e.g., during respiration, with sweating, and in feces). The kidneys are the only regulated route of water excretion. Excretion of water by the kidneys is regulated by AVP secreted from the posterior pituitary. When AVP levels are high, the kidneys excrete a small volume of hyperosmotic urine. When AVP levels are low, a large volume of hypoosmotic urine is excreted.
2.