In the kidney, the macula densa is an area of closely packed specialized cells lining the wall of the distal tubule 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 concentration of sodium chloride in
the distal convoluted tubule. A decrease in
sodium chloride concentration initiates a
signal from the macula densa that has two
effects: (1) it decreases resistance to blood flow in the afferent arterioles, which
increases glomerular hydrostatic pressure
and helps return glomerulus filtration rate
(GFR) toward normal, and (2) it increases renin release from the juxtaglomerular cells of the afferent and efferent arterioles,
which are the major storage sites for renin. [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 are taller and
have more prominent nuclei than surrounding cells of the distal straight
tubule (cortical thick ascending limb). The close proximity and prominence of the
nuclei cause this segment of the distal
tubule wall to appear darker in microscopic preparations,[2] 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 A decrease in blood pressure causes a decrease in the GFR (glomerular filtration
rate) which causes more reabsorption,
resulting in a decreased concentration of
sodium and chloride ions in the filtrate
and/or decreased filtrate flow rate that the
macula densa can sense and then trigger an autoregulatory response to increase
reabsorption of ions and water in order to
return blood pressure to normal. Reduced
blood pressure means decreased venous
pressure and hence a decreased peritubular capillary pressure. This causes a smaller capillary hydrostatic pressure which causes an increased absorption of sodium ions
into the vasa recta at the proximal tubule. Because of this increased absorption, less
NaCl is present at the distal tubule which is where the macula densa is located. The
macula densa senses this drop in salt
concentration and responds through two
mechanisms: first, it triggers dilation of the
renal afferent arteriole, decreasing
afferent arteriole resistance and thus offsetting the decrease in glomerular
hydrostatic pressure caused by the drop in
blood pressure. Second, macula densa cells
release prostaglandins, which triggers granular juxtaglomerular cells lining the afferent arterioles to release renin into the bloodstream. (The juxtaglomerular 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. The process triggered by the Macula densa
helps keep the glomerular filtration rate (GFR) fairly steady in response to varying
artery pressure, due to dilation of the afferent arterioles and the action of Renin, which triggers constriction of the efferent arterioles, both of which increase hydrostatic pressure in the glomerulus.
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