The integration of the different control systems that regulate sodium and fluid excretion under normal conditions can be summarized by examining the homeostatic responses to progressive increases in dietary sodium intake. As discussed previously, the kidneys have an amazing capability to match their excretion of salt and water to intakes that can range from as low as one tenth of normal to as high as 10 times normal.

High Sodium Intake Suppresses Antinatriuretic Systems and Activates Natriuretic Systems. As sodium intake is increased, sodium output initially lags slightly behind intake. The time delay results in a small increase in the cumulative sodium balance, which causes a slight increase in extracellular fluid volume. It is mainly this small increase in extracellular fluid volume that triggers various mechanisms in the body to increase sodium excretion. These mechanisms include the following:

1. Activation of low-pressure receptor reflexes that originate from the stretch receptors of the right atrium and the pulmonary blood vessels. Signals from the stretch receptors go to the brain stem and there inhibit sympathetic nerve activity to the kidneys to decrease tubular sodium reabsorption. This mechanism is most important in the first few hours—or perhaps the first day—after a large increase in salt and water intake.

 2. Suppression of Ang II formation, caused by increased arterial pressure and extracellular fluid volume expansion, decreases tubular sodium reabsorption by eliminating the normal effect of Ang II to increase sodium reabsorption. Also, reduced Ang II decreases aldosterone secretion, thus further reducing tubular sodium reabsorption.

3. Stimulation of natriuretic systems, especially ANP, contributes further to increased sodium excretion. Thus, the combined activation of natriuretic systems and suppression of sodium- and water-retaining systems leads to an increase in sodium excretion when sodium intake is increased. The opposite changes take place when sodium intake is reduced below normal levels.

4. Small increases in arterial pressure, caused by volume expansion, may occur with large increases in sodium intake; this mechanism raises sodium excretion through pressure natriuresis. As dis cussed previously, if the nervous, hormonal, and intrarenal mechanisms are operating effectively, measurable increases in blood pressure may not occur even with large increases in sodium intake over several days. However, when high sodium intake is sustained for months or years, the kidneys may become damaged and less effective in excreting sodium, necessitating increased blood pressure to maintain sodium balance through the pressure natriuresis mechanism.

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مواضيع ذات صلة

Conditions That Cause Large Increases in Blood Volume and Extracellular Fluid Volume

Role of Atrial Natriuretic Peptide in Controlling Renal Excretion

Role of Aldosterone in Controlling Renal Excretion

Role of Ang II in Controlling Renal Excretion

Sympathetic Nervous System Control of Renal Excretion: Arterial Baroreceptor and Low-Pressure Stretch Receptor Reflexes

Importance of Pressure Natriuresis and Pressure Diuresis in Maintaining Body Sodium and Fluid Balance

Integration of Renal Mechanisms for Control of Extracellular Fluid

Osmoreceptor-ADH Feedback System

Urine Specific Gravity

Renal Mechanisms for Excreting Dilute Urine

Physiological Control of Glomerular Filtration and Renal Blood Flow

Renal Blood Flow