Macula densa

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Macula densa

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In the kidney, the macula densa is an area of closely packed specialized cells lining the wall of the thick ascending limb of Henle (TALH) at the point of return of the nephron to the vascular pole of its parent glomerulus glomerular vascular pole.

The cells of the macula densa are sensitive to the ionic content and water volume of the fluid in the TALH, producing molecular signals that promote renin secretion by other cells of the juxtaglomerular apparatus.[1] The release of renin is an essential component of the renin-angiotensin-aldosterone system (RAAS), which regulates blood pressure and volume.

Histology

The cells of the macula densa cells are taller and have more prominent nuclei than surrounding cells of the thick ascending limb of Henle.

The close proximity and prominence of the nuclei cause this segment of the TALH wall to appear darker in microscopic preparations[1], hence the name macula densa.

Function

Schematic depicting how the RAAS works. Here, activation of the RAAS is initiated by a low perfusion pressure in the juxtaglomerular apparatus
Schematic depicting how the RAAS works. Here, activation of the RAAS is initiated by a low perfusion pressure in the juxtaglomerular apparatus

A decrease in blood pressure results in a decreased concentration of sodium and chloride ions at the macula densa. (This is due to reduced filtration by the glomerulus: less filtrate is expelled into Bowman's space and the proximal convoluted tubule; the resulting fluid reaching the macula will have a lower sodium chloride concentration after the sodium chloride is removed along the thick ascending limb of Henle.)

In response, the macula densa cells release prostaglandins, which triggers granular juxtaglomerular cells lining the afferent arterioles to release renin into the bloodstream. (The juxtoglomerular cells can also release renin independently of the macula densa, as they are also triggered by baroreceptors lining the arterioles, and release renin if a fall in blood pressure in the arterioles is detected.) Furthermore, activation of the sympathetic nervous system stimulates renin release through activation of beta-1 receptors.

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Acknowledgement and Attribution Regarding Sources of Content

Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .

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