Ganong's Review of Medical Physiology, 23rd Edition

CHAPTER 22The Adrenal Medulla & Adrenal Cortex 359

ROLE OF MINERALOCORTICOIDS

IN THE REGULATION OF

SALT BALANCE

Variation in aldosterone secretion is only one of many factors
affecting Na+ excretion. Other major factors include the glo-
merular filtration rate, ANP, the presence or absence of os-
motic diuresis, and changes in tubular reabsorption of Na+
independent of aldosterone. It takes some time for aldoster-

one to act. When one rises from the supine to the standing po-

sition, aldosterone secretion increases and Na+ is retained

from the urine. However, the decrease in Na+ excretion devel-

ops too rapidly to be explained solely by increased aldosterone

secretion. The primary function of the aldosterone-secreting

mechanism is the defense of intravascular volume, but it is

only one of the homeostatic mechanisms involved.

SUMMARY OF THE EFFECTS OF

ADRENOCORTICAL HYPER- &

HYPOFUNCTION IN HUMANS

Recapitulating the manifestations of excess and deficiency of

the adrenocortical hormones in humans is a convenient way

to summarize the multiple and complex actions of these ster-

oids. A characteristic clinical syndrome is associated with ex-

cess secretion of each of the types of hormones.

Excess androgen secretion causes masculinization (adreno-

genital syndrome) and precocious pseudopuberty or female

pseudohermaphroditism.

Excess glucocorticoid secretion produces a moon-faced,

plethoric appearance, with trunk obesity, purple abdominal

striae, hypertension, osteoporosis, protein depletion, mental

abnormalities, and, frequently, diabetes mellitus (Cushing

syndrome). The causes of Cushing syndrome have been dis-

cussed previously.

Excess mineralocorticoid secretion leads to K+ depletion and

Na+ retention, usually without edema but with weakness,

hypertension, tetany, polyuria, and hypokalemic alkalosis

(hyperaldosteronism). This condition may be due to primary

adrenal disease (primary hyperaldosteronism; Conn syn-

drome) such as an adenoma of the zona glomerulosa, unilateral

or bilateral adrenal hyperplasia, adrenal carcinoma, or GRA. In

patients with primary hyperaldosteronism, renin secretion is

depressed. Secondary hyperaldosteronism with high plasma

renin activity is caused by cirrhosis, heart failure, and nephro-

sis. Increased renin secretion is also found in individuals with

the salt-losing form of the adrenogenital syndrome (see above),

because their ECF volume is low. In patients with elevated renin

secretion due to renal artery constriction, aldosterone secretion

is increased; in those in whom renin secretion is not elevated,

aldosterone secretion is normal. The relationship of aldoster-

one to hypertension is discussed in Chapter 33.

FIGURE 22–26 Effect of low-, normal-, and high-sodium
diets on sodium metabolism and plasma renin activity,
aldosterone, vasopressin, and ANP in normal humans. (Data from
Sagnella GA, et al: Plasma atrial natriuretic peptide: Its relationship to changes in
sodium in-take, plasma renin activity, and aldosterone in man. Clin Sci 1987;72:25.)

150

140

130

120

15

10

400

300

200

100

2000

0

1500

1000

500

0

15

20

10

5

0

5

0

2.0

2.5

1.5

1.0

0.5

0

Low Normal High

Sodium intake

Plasma vasopressin

(pg/mL)

Plasma renin activity

(ng A

I/mL/h)

Plasma Na

+

(mmol/L)

Plasma aldosterone

(pmol/L)

Urinary Na

+

excretion(mmol/day)

Plasma ANP

(pg/mL)

TABLE 22–7 Second messengers involved

in the regulation of aldosterone secretion.

Secretagogue Intracellular Mediator

ACTH Cyclic AMP, protein kinase A

Angiotensin II Diacylglycerol, protein kinase C

K+ Ca2+ via voltage-gated Ca2+ channels