Aldosterone increases sodium reabsorption, especially in the cortical collecting tubules. The increased sodium reabsorption is also associated with increased water reabsorption and potassium secretion. Therefore, the net effect of aldosterone is to make the kidneys retain sodium and water but also to increase potassium excretion in the urine.

The function of aldosterone in regulating sodium balance is closely related to that described for Ang II. That is, with reduction in sodium intake, the increased Ang II levels that occur stimulate aldosterone secretion, which in turn contributes to the reduction in urinary sodium excretion and, therefore, to the maintenance of sodium balance. Conversely, with high sodium intake, suppression of aldosterone formation decreases tubular reabsorption, allowing the kidneys to excrete larger amounts of sodium. Thus, changes in aldosterone formation also aid the pressure natriuresis mechanism in maintaining sodium balance during variations in salt intake.

During Chronic Oversecretion of Aldosterone, the Kidneys “Escape” from Sodium Retention as Arterial Pressure Rises. Although aldosterone has powerful effects on sodium reabsorption, when there is excessive infusion of aldosterone or excessive formation of aldosterone, as occurs in patients with tumors of the adrenal gland (Conn’s syndrome), the increased sodium reabsorption and decreased sodium excretion by the kidneys are transient. After 1 to 3 days of sodium and water retention, the extra cellular fluid volume rises by about 10 to 15 percent and there is a simultaneous increase in arterial blood pressure. When the arterial pressure rises sufficiently, the kidneys “escape” from the sodium and water retention and thereafter excrete amounts of sodium equal to the daily intake, despite the continued presence of high levels of aldosterone. The primary reason for the escape is the pressure natriuresis and diuresis that occur when the arterial pressure rises.

In patients with adrenal insufficiency who do not secrete enough aldosterone (Addison’s disease), there is increased excretion of sodium and water, reduction in extracellular fluid volume, and a tendency toward low blood pressure. In the complete absence of aldosterone, the volume depletion may be severe unless the person is allowed to eat large amounts of salt and drink large amounts of water to balance the increased urine output of salt and water.

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مواضيع ذات صلة

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

Determinants of The GFR

Glomerular Filtration—The First Step in Urine Formation

Urine Formation Results From Glomerular Filtration, Tubular Reabsorption, and Tubular Secretion