The macula densa ◦ Regulation the GFRYou might want to check out the nephron overview and glomerular filtration entries.

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The macula densa

As the distal proximal tubule rises indigenous the renal medulla, it renders close call with the glomerulus. The cells on the side of the tubule encountering the glomerulus have a distinctive appearance and constitute the macular densa (Figure 1). This cells sense the NaCl content of the tubule and make changes to GFR appropriately.


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Figure 1: The macula densa is a region of specialised cell lining the distal convoluted tubule. It monitors tubular NaCl concentrations and also adjusts glomerular filtration accordingly. That is ideally located close to the afferent arteriole which governs glomerular filtration and the granular cell which surround the afferent arteriole and also secrete renin when as necessary stimulated.

A high concentration the NaCl in distal tubular liquid usually results from an extreme glomerular filtration price (GFR), such that there is not time for the NaCl to be reabsorbed in the renal tubules. Under these circumstances, macula densa cells relax adenosine, i m sorry constricts the surrounding afferent arteriole, to reduce glomerular perfusion and also hence GFR.

On the other hand, low tubular NaCl usually results from excessive reabsorption because GFR is low. As soon as this occurs, the macular densa cells relax prostaglandin E2 (PGE2), which triggers relax of renin from the granular cell (AKA juxtaglomerular cells) surrounding the afferent arteriole together it enters the glomerulus. Renin relax activates the renin-angiotensin system raising blood pressure and consequently renal perfusion.

Another means to think around GFR and also NaCl reabsorption is to photo the renal tubule together a lengthy conveyor belt shifting NaCl v the nephron. Pumps and transporters shot to reabsorb sodium (like employees removing items native a conveyor belt in a factory) as it moves along. Once the conveyor belt is moving gradually (low GFR) it is straightforward to take every bit of NaCl off the conveyor belt prior to it reaches the end (the macula densa). However, if the conveyor belt is relocating too easily (high GFR), some of the NaCl is left top top the belt at the end. By increasing or slowing down the conveyor belt (GFR) you control the lot of NaCl top top it at the end.

NaCl and GFR adjustments

The exact molecular details of precisely how transforms in NaCl bring about adenosine or PGE2 release room still incompletely understood and also the topic of continuous research. Accumulation of Na+ in macular densa cells leads to relax of adenosene (or ATP, which subsequently breaks under to adenosine), due to cell swelling together water follows excess Na+ right into cells (Figure 2). The specific mechanism linking cellular ede to adenosine/ATP release is not specific at present. Just how reduced intracellular NaCl is detect by macula densa cells and leads come PGE2 manufacturing is not well characterized at present. One watch holds the it is intracellular Cl- the is the trigger. PGE2 is known to be created by cyclooxygenase-2, yet just just how the activity of this enzyme is regulated by Cl- (or Na+) isn"t clear.

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Figure 2: figure 2: NaCl sensing and responses by macular densa cells. Under regular circumstances, Na+ is pumped into macula densa cells from the tubular lumen through the Na+/K+/Cl- cotransporter, and out the the basal surface of the cells via the Na+/K+ ATPase pump. When tubular Na+ is high, Na+ beginning the cells at a price which saturates the Na+/K+ ATPase pump, so that Na+ accumulates within the cells. This reasons cell swelling and adenosine (or ATP which subsequently breaks under to adenosine) is released, constricting the surrounding afferent artery, reduce GFR. By contrast, once tubular NaCl is low, the intracellular concentration if NaCl is decreased in macula densa cells PGE2 is released, resulting in renin release from granular cell, enhancing blood push (and hence, GFR) via the renin-angiotensin system.