Macula Densa - Function

Function

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. The macula densa can sense this decrease and trigger an autoregulatory response to further 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 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.