Briefly describe and explain the physiological consequences of excessive aldosterone secretion.

Outline:

·        Actions of aldosterone on:

- plasma sodium

- potassium secretion

- H⁺ secretion

·        Effects of excessive aldosterone:

- K⁺ depletion

- Hypertension and volume expansion

Essay:

            Aldosterone is a steroid hormone synthesized by the zona glomerulosa of the adrenal cortex. The principal function of aldosterone is to sustain extracellular fluid (ECF) volume by conserving body sodium.

            The kidney is the major site of aldosterone activity. Aldosterone stimulates the active reabsorption of sodium from the tubular urine back into the nearby capillaries by collecting duct and late distal convoluted tubule cells. Thus, net urinary sodium excretion is diminished. Because water is passively reabsorbed with sodium, there is little increase in plasma sodium concentration.

            Aldosterone acts at the apical surface of renal tubular cells to increase the number of membrane sodium channels and at the basolateral membrane to increase Na⁺-K⁺-ATPase, which pumps the sodium out. Aldosterone stimulates the active secretion of potassium out of the tubular cell and into the urine concurrently with sodium reabsorption. Most of the potassium that is excreted daily results from distal tubular secretion. Hence, aldosterone is critical for the disposal of daily dietary potassium load at a normal plasma potassium concentration. Aldosterone also enhances tubular secretion of hydrogen ions as sodium is reabsorbed.

            The common cause of excessive aldosterone secretion is a primary tumor in the aldosterone-secreting cells of the adrenal cortex or due to obstructive lesions of the renal arteries, which reduce perfusion pressure, stimulate excess renin and therefore aldosterone secretion. One serious physiological consequence is increased loss of potassium ions in the urine, leading to potassium depletion. Hypokalemia itself hyperpolarizes the membrane potential, thereby reducing excitability, leading to muscular weakness and eventual cardiac failure. Prolonged potassium depletion damages the kidneys, resulting in a loss of concentrating ability and polyuria. The potassium depletion also causes muscle weakness and metabolic alkalosis, and the alkalosis lowers the plasma calcium level to the point where tetany is present.

            Excessive aldosterone secretion produces sodium retention, weight gain, and an increase in blood pressure as a result of the expanded ECF volume. When the ECF expands beyond a certain point, sodium retention stops and its excretion is increased due to secretion of ANP.