The principal mineralocorticoid action is enhancement of Na+ reabsorption in the distal convoluted tubule in kidney. There is an associated increase in K+ and H+ excretion.
MINERALOCORTICOID ACTIONS
The
principal mineralocorticoid action is enhancement of Na+ reabsorption in the
distal convoluted tubule in kidney. There is an associated increase in K+ and
H+ excretion. Its deficiency results in decreased maximal tubular reabsorptive
capacity for Na+; kidney is not able to retain Na+ even in the Na+ deficient
state → Na+ is progressively
lost: kidneys absorb water without attendant Na+ (to maintain e.c.f. volume
which nevertheless decreases) → dilutional hyponatraemia → excess water enters
cells → cellular hydration:
decreased blood volume and raised haematocrit. Hyperkalaemia and acidosis accompany.
These distortions of fluid and electrolyte balance progress and contribute to
circulatory collapse. Thus, these actions make adrenal cortex essential for
survival.
Similar action on
cation transport is exerted in other tissues also. The action of aldosterone is
expressed by gene mediated increased transcription of mRNA in renal tubular
cells which directs synthesis of proteins (aldosteroneinduced proteins—AIP).
The Na+K+ ATPase of tubular basolateral membrane responsible for generating
gradients for movement of cations in these cells is the major AIP (see Fig. 41.3). Synthesis of subunit of
amiloride sensitive Na+ channel is also induced. Because of the time taken to
induce protein synthesis, aldosterone has a latency of action of 1–2 hours. In
addition, aldosterone rapidly induces phosphorylation and activation of
amiloride sensitive Na+ channel.
The
main adverse effect of excessive mineralocorticoid action is fluid retention
and hypertension. The natural and some of the synthetic glucocorticoids have
significant mineralocorticoid activity responsible for side effects like edema,
progressive rise in BP, hypokalemia and alkalosis. The diuretic induced
hypokalemia is aggravated.
Aldosterone has been
shown to promote CHF associated myocardial fibrosis and progression of the disease.
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