Aldosterone: Difference between revisions
No edit summary |
No edit summary |
||
| Line 6: | Line 6: | ||
Unlike [[neuroreceptor]]s, classic [[steroid]] receptors are intracellularly located. The aldosterone/MR receptor complex binds on the DNA to specific [[hormone response element]], which leads to gene specific [[transcription (genetics)|transcription]]. Some of the transcribed genes are crucial for [[transepithelial sodium transport]], including the three [[subunit]]s of the [[epithelial sodium channel]], the [[Na+/K+-ATPase|Na<sup>+</sup>/K<sup>+</sup> pumps]] and their regulatory proteins [[serum and glucocorticoid-induced kinase]], and [[channel-inducing factor]] respectively. |
Unlike [[neuroreceptor]]s, classic [[steroid]] receptors are intracellularly located. The aldosterone/MR receptor complex binds on the DNA to specific [[hormone response element]], which leads to gene specific [[transcription (genetics)|transcription]]. Some of the transcribed genes are crucial for [[transepithelial sodium transport]], including the three [[subunit]]s of the [[epithelial sodium channel]], the [[Na+/K+-ATPase|Na<sup>+</sup>/K<sup>+</sup> pumps]] and their regulatory proteins [[serum and glucocorticoid-induced kinase]], and [[channel-inducing factor]] respectively. |
||
Aldosterone synthesis is stimulated by increased [[blood plasma|plasma]] [[angiotensin II]], [[ACTH]], 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 |
Aldosterone synthesis is stimulated by increased [[blood plasma|plasma]] [[angiotensin II]], [[ACTH]], 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.<ref>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. [http://jap.physiology.org/cgi/content/full/96/4/1406 Full Text]</ref> |
2004 J Appl Physiol 96: 1406-1414. [http://jap.physiology.org/cgi/content/full/96/4/1406 Full Text]</ref> |
||
Revision as of 01:31, 28 November 2006
Aldosterone is a steroid hormone (mineralocorticoid family) 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 in human (corticosterone in rodent). 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 specific hormone response element, which leads to gene specific transcription. Some of the transcribed genes are crucial for transepithelial sodium transport, including the three subunits of the epithelial sodium channel, the Na+/K+ pumps and their regulatory proteins serum and glucocorticoid-induced kinase, and channel-inducing factor respectively.
Aldosterone synthesis is stimulated by increased plasma angiotensin II, ACTH, 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.[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.
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
- ^ Brenner & Rector's The Kidney, 7th ed. Saunders, 2004.
- ^ Sherwood, L. Human Physiology, from Cells to Systems, 4th Ed., Brooks/Cole, 2001
- ^ 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.