How Plasma Proteins Slows Elimination Of Cortisol

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Glucocorticoid and mineralocorticoid activities of the steroids are relative to Cortisol, with Cortisol being 1.0.

• Cortisol (very slight mineralocorticoid activity, but large quantity secreted)

• Cortisone (synthetic, slight mineralocorticoid activity)

Glucocorticoids

• Cortisol (very potent, accounts for about 95 per cent of all glucocorticoid activity)

• Corticosterone (provides about 4 per cent of total glucocorticoid activity, but much less potent than cortisol)

• Cortisone (synthetic, almost as potent as cortisol)

• Prednisone (synthetic, four times as potent as cortisol)

• Methylprednisone (synthetic, five times as potent as cortisol)

• Dexamethasone (synthetic, 30 times as potent as cortisol)

It is clear from this list that some of these hormones have both glucocorticoid and mineralocorticoid activities. It is especially significant that cortisol has a small amount of mineralocorticoid activity, because some syndromes of excess cortisol secretion can cause significant mineralocorticoid effects, along with its much more potent glucocorticoid effects.

The intense glucocorticoid activity of the synthetic hormone dexamethasone, which has almost zero mineralocorticoid activity, makes this an especially important drug for stimulating specific glucocorticoid activity.

Adrenocortical Hormones Are Bound to Plasma Proteins.

Approximately 90 to 95 per cent of the cortisol in the plasma binds to plasma proteins, especially a globulin called cortisol-binding globulin or transcortin and, to a lesser extent, to albumin. This high degree of binding to plasma proteins slows the elimination of cortisol from the plasma; therefore, cortisol has a relatively long halflife of 60 to 90 minutes. Only about 60 per cent of circulating aldosterone combines with the plasma proteins, so that about 40 per cent is in the free form; as a result, aldosterone has a relatively short half-life of about 20 minutes. In both the combined and free forms, the hormones are transported throughout the extracellular fluid compartment.

Binding of adrenal steroids to the plasma proteins may serve as a reservoir to lessen rapid fluctuations in free hormone concentrations, as would occur, for example, with cortisol during brief periods of stress and episodic secretion of ACTH. This reservoir function may also help to ensure a relatively uniform distribution of the adrenal hormones to the tissues.

Adrenocortical Hormones Are Metabolized in the Liver. The adrenal steroids are degraded mainly in the liver and conjugated especially to glucuronic acid and, to a lesser extent, sulfates. These substances are inactive and do not have mineralocorticoid or glucocorticoid activity. About 25 per cent of these conjugates are excreted in the bile and then in the feces. The remaining conjugates formed by the liver enter the circulation but are not bound to plasma proteins, are highly soluble in the plasma, and are therefore filtered readily by the kidneys and excreted in the urine. Diseases of the liver markedly depress the rate of inactivation of adrenocortical hormones, and kidney diseases reduce the excretion of the inactive conjugates.

The normal concentration of aldosterone in blood is about 6 nanograms (6 billionths of a gram) per 100 ml, and the average secretory rate is approximately 150 |ig/day (0.15 mg/day).

The concentration of cortisol in the blood averages 12 | g/100 ml, and the secretory rate averages 15 to 20 mg/day.

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