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Chapter: Medical Physiology: Renal Regulation of Potassium, Calcium, Phosphate, and Magnesium; Integration of Renal Mechanisms for Control of Blood Volume and Extracellular Fluid Volume

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Integrated Responses to Changes in Sodium Intake

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.

Integrated Responses to Changes in Sodium Intake

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 isincreased, 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 trig-gers various mechanisms in the body to increase sodium excretion. These mechanisms include the following:

1.      Activation of low pressure receptor reflexes thatoriginate 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.     Small increases in arterial pressure, caused byvolume expansion, raise sodium excretion through pressure natriuresis.

 

3.     Suppression of angiotensin II formation, caused byincreased arterial pressure and extracellular fluid volume expansion, decreases tubular sodium reabsorption by eliminating the normal effect of angiotensin II to increase sodium reabsorption.

 Also, reduced angiotensin II decreases aldosterone secretion, thus further reducing tubular sodium reabsorption.


4.     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.


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