Negative feedback mechanism regulating the glomerular filtration rate
In the physiology of the kidney, tubuloglomerular feedback (TGF) is a feedback system inside the kidneys. Within each nephron, information from the renal tubules (a downstream area of the tubular fluid) is signaled to the glomerulus (an upstream area). Tubuloglomerular feedback is one of several mechanisms the kidney uses to regulate glomerular filtration rate (GFR). It involves the concept of purinergic signaling, in which an increased distal tubular sodium chloride concentration causes a basolateral release of adenosine from the macula densa cells. This initiates a cascade of events that ultimately brings GFR to an appropriate level.[1][2][3]
^Arulkumaran N, Turner CM, Sixma ML, Singer M, Unwin R, Tam FW (1 January 2013). "Purinergic signaling in inflammatory renal disease". Frontiers in Physiology. 4: 194. doi:10.3389/fphys.2013.00194. PMC 3725473. PMID 23908631. Extracellular adenosine contributes to the regulation of GFR. Renal interstitial adenosine is mainly derived from dephosphorylation of released ATP, AMP, or cAMP by the enzyme ecto-5′-nucleotidase (CD73) (Le Hir and Kaissling, 1993). This enzyme catalyzes the dephosphorylation of 5′-AMP or 5′-IMP to adenosine or inosine, respectively, and is located primarily on the external membranes and mitochondria of proximal tubule cells, but not in distal tubule or collecting duct cells (Miller et al., 1978). ATP consumed in active transport by the macula densa also contributes to the formation of adenosine by 5- nucleotidase (Thomson et al., 2000). Extracellular adenosine activates A1 receptors on vascular afferent arteriolar smooth muscle cells, resulting in vasoconstriction and a reduction in GFR (Schnermann et al., 1990).
^Praetorius HA, Leipziger J (1 March 2010). "Intrarenal purinergic signaling in the control of renal tubular transport". Annual Review of Physiology. 72 (1): 377–93. doi:10.1146/annurev-physiol-021909-135825. PMID 20148681.
^Persson AE, Lai EY, Gao X, Carlström M, Patzak A (1 January 2013). "Interactions between adenosine, angiotensin II and nitric oxide on the afferent arteriole influence sensitivity of the tubuloglomerular feedback". Frontiers in Physiology. 4: 187. doi:10.3389/fphys.2013.00187. PMC 3714451. PMID 23882224.
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