Drugs & Medication

Aldosterone is a steroid hormone produced by the outer-section (zona glomerulosa) of the adrenal cortex in the adrenal gland to regulate sodium and potassium balance in the blood. It is synthesized from cholesterol by aldosterone synthase, which is absent in other sections of the adrenal gland. It is the sole endogenous member of the class of mineralocorticoids. Acting on mineralocorticoid receptors (MR) on principal cells in the distal tubule of the kidney nephron, it increases the permeability of their apical (luminal) membrane to potassium and sodium and activates their basolateral Na+/K+ pumps, stimulating ATP hydrolysis, reabsorbing sodium (Na+) ions and water into the blood, and excreting potassium (K+) ions into the urine. Aldosterone also stimulates H+ secretion by α-intercalated cells in the collecting duct, regulating plasma bicarbonate (HCO3⁻) levels and its acid/base balance.^[1]

Aldosterone is responsible for the reabsorption of about 2% of filtered sodium in the kidneys, which is nearly equal to the entire sodium content in human blood under normal GFR (glomerular filtration rate).^[2]

Unlike neuroreceptors, classic steroid receptors are intracellularly located. The aldosterone/MR receptor complex binds on the DNA to the hormone response element, which alters protein synthesis and the transcription of messenger RNA. Some of the transcribed genes are important for transepithelial sodium transport, including serum and glucocorticoid-induced kinase, channel-inducing factor, K-ras2A, and three subunits of the epithelial sodium channel.

Aldosterone synthesis is stimulated by increased plasma angiotensin II or potassium levels, which are present in proportion to plasma sodium deficiencies. It is also stimulated by plasma acidosis. The secretion of aldosterone has a diurnal rhythm; about 75% of the daily production is secreted between 04:00 am and 10:00 am each day.^[3]

Aldesterone release is also stimulated by the stretch receptors located in the atria of the heart. If decreased blood pressure is detected, the adrenal gland is stimulated by these stretch receptors to release aldesterone, which increases sodium reabsorption from the urine, sweat and the gut. This causes increased osmolarity in the extracellular fluid which will eventually return blood pressure toward normal.

Contents 1 Aldosterone and the kidney 1.1 Control of aldosterone release 2 References

Aldosterone and the kidney

Control of aldosterone release

• The role of the renin-angiotensin system
  The role of sympathetic nerves
  The role of baroreceptors
  The role of the juxtaglomerular apparatus
  The plasma concentration of potassium

References

1. ^ Brenner & Rector's The Kidney, 7th ed. Saunders, 2004.
2. ^ Sherwood, L. Human Physiology, from Cells to Systems, 4th Ed., Brooks/Cole, 2001
3. ^ Hurwitz S, Cohen R, & Williams GH. Diurnal variation of aldosterone and plasma renin activity: timing relation to melatonin and cortisol and consistency after prolonged bed rest. 2004 J Appl Physiol 96: 1406-1414. Full Text

• Williams JS, Williams GH. 50th anniversary of aldosterone. J Clin Endocrinol Metab. 2003 Jun;88(6):2364-72. Full text. PMID 12788829.