The Kidneys Play a Dominant Role in Regulating Na1 Balance

Figure 24.11 summarizes Na+ balance throughout the body. Dietary intake of Na+ varies and, in a typical American diet, amounts to about 100 to 300 mEq/day, mostly in the form of NaCl. Ingested Na+ is mainly absorbed in the small intestine and is added to the ECF, where it is the major determinant of the osmolality and the amount of water in (or volume of) this fluid compartment. About 50% of the body's Na+ is in the ECF, about 40% in bone, and about 10% within cells.

Losses of Na+ occur via the skin, gastrointestinal tract, and kidneys. Skin losses are usually small, but can be considerable with sweating, burns, or hemorrhage. Likewise, gastrointestinal losses are usually small, but they can be large and serious with vomiting, diarrhea, or iatrogenic suction or drainage of gastrointestinal secretions. The kidneys are ordinarily the major routes of Na+ loss from the body, excreting about 95% of the ingested Na+ in a healthy person. Thus, the kidneys play a dominant role in the control of Na+ balance. The kidneys can adjust Na+ excretion over a wide range, reducing it to low levels when there is a Na+ deficit and excreting more Na+ when there is Na+ excess in the body. Adjustments in Na+ excretion occur by engaging many of the factors previously discussed.

Regulated variable

Ecf Volume And Diarrhea

Na+ balance. Most of the Na+ consumed in our diets is excreted by the kidneys.

Regulated variable

Volume Regulation Baroreceptor

The regulation of ECF volume or effective arterial blood volume (EABV) by a negative-feedback control system. Arterial baroreceptors and the kidneys sense the degree of fullness of the arterial system. The kidneys are the effectors, and they change Na+ excretion to restore EABV to normal.

Na+ balance. Most of the Na+ consumed in our diets is excreted by the kidneys.

The regulation of ECF volume or effective arterial blood volume (EABV) by a negative-feedback control system. Arterial baroreceptors and the kidneys sense the degree of fullness of the arterial system. The kidneys are the effectors, and they change Na+ excretion to restore EABV to normal.

In a healthy individual, one can think of the ECF volume as the regulated variable in a negative-feedback control system (Fig. 24.12). The kidneys are the effectors, and they change Na+ excretion in an appropriate manner. An increase in ECF volume promotes renal Na+ loss, which restores a normal volume. A decrease in ECF volume leads to decreased renal Na+ excretion, and this Na+ retention (with continued dietary Na+ intake) leads to the restoration of a normal ECF volume. Closer examination of this concept, particularly when considering pathophysiological states, however, suggests that it is of limited usefulness. A more considered view suggests that the effective arterial blood volume (EABV) is actually the regulated variable. In a healthy individual, ECF volume and EABV usually change together in the same direction. In an abnormal condition such as congestive heart failure, however, EABV is low when the ECF volume is abnormally increased. In this condition, there is a potent stimulus for renal Na+ retention that clearly cannot be the ECF volume.

When EABV is diminished, the degree of fullness of the arterial system is less than normal and tissue blood flow is inadequate. Arterial baroreceptors in the carotid sinuses and aortic arch sense the decreased arterial stretch. This will produce reflex activation of sympathetic nerve fibers to the kidneys, with consequently decreased GFR and renal blood flow and increased renin release. These changes favor renal Na+ retention. Reduced EABV is also "sensed" in the kidneys in three ways:

1) A low pressure at the level of the afferent arteriole stimulates renin release via the intrarenal baroreceptor mechanism.

2) Decreases in renal perfusion pressure lead to a reduced GFR and, hence, diminished Na+ excretion.

3) Decreases in renal perfusion pressure will also reduce peritubular capillary hydrostatic pressure, increasing the uptake of reabsorbed fluid and diminishing Na+ excretion.

When kidney perfusion is threatened, the kidneys retain salt and water, a response that tends to improve their perfusion.

In several important diseases, including heart and liver and some kidney diseases, abnormal renal retention of Na+ contributes to the development of generalized edema, a widespread accumulation of salt and water in the interstitial spaces of the body. The condition is often not clinically evident until a person has accumulated more than 2.5 to 3 L of ECF in the interstitial space. Expansion of the interstitial space has two components: (1) an altered balance of Starling forces exerted across capillaries, and (2) the retention of extra salt and water by the kidneys. Total plasma volume is only about 3.5 L,- if edema fluid were derived solely from the plasma, hemoconcentration and circulatory shock would ensue. Conservation of salt and water by the kidneys is clearly an important part of the development of generalized edema.

Patients with congestive heart failure may accumulate many liters of edema fluid, which is easily detected as weight gain (since 1 L of fluid weighs 1 kg). Because of the effect of gravity, the ankles become swollen and pitting edema develops. As a result of heart failure, venous pressure is elevated, causing fluid to leak out of the capillaries because of their elevated hydrostatic pressure. Inadequate pumping of blood by the heart leads to a decrease in EABV, so the kidneys retain salt and water. Alterations in many of the factors discussed above—decreased GFR, increased RAAS activity, changes in intrarenal physical forces, and increased sympathetic nervous system activity—contribute to the renal salt and water retention. To minimize the accumulation of edema fluid, patients are often placed on a reduced Na+ intake and given diuretic drugs.

Hypertension may often be a result of a disturbance in NaCl (salt) balance. Excessive dietary intake of NaCl or inadequate renal excretion of salt tends to increase intravas-cular volume, this change translates into an increase in blood pressure. A reduced salt intake, ACE inhibitors, diuretic drugs, or drugs that more directly affect the cardiovascular system (e.g., Ca2+ channel blockers or (3-adrener-gic blockers) are useful therapies in controlling hypertension in many people.

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Responses

  • szymon hamilton
    Is na a variable that is regulated by the kidneys?
    7 years ago

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