Premium
Mediators of tubuloglomerular feedback regulation of glomerular filtration: ATP and adenosine
Author(s) -
Castrop H.
Publication year - 2007
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/j.1748-1716.2006.01610.x
Subject(s) - tubuloglomerular feedback , macula densa , afferent arterioles , adenosine , glomerulus , juxtaglomerular apparatus , nephron , chemistry , medicine , microbiology and biotechnology , loop of henle , endocrinology , tubular fluid , purinergic signalling , kidney , biology , reabsorption , angiotensin ii , biochemistry , renin–angiotensin system , adenosine receptor , receptor , blood pressure , agonist
In the juxtaglomerular apparatus of the kidney the loop of Henle gets into close contact to its parent glomerulus. This anatomical link between the tubular system and the vasculature of the afferent and efferent arteriole enables specialized tubular cells, the macula densa (MD) cells, to establish an intra‐nephron feedback loop designed to control preglomerular resistance and thereby single nephron glomerular filtration rate. This review focuses on the signalling mechanisms which link salt‐sensing MD cells and the regulation of preglomerular resistance, a feedback loop known as tubuloglomerular feedback (TGF). Two purinergic molecules, ATP and adenosine, have emerged over the years as most likely candidates to serve as mediators of TGF. Data will be reviewed supporting a role of either ATP or adenosine as mediators of TGF. In addition, a concept will be discussed that integrates both ATP and adenosine into one signalling cascade that includes (i) release of ATP from MD cells upon increases in tubular salt concentration, (ii) extracellular degradation of ATP to form adenosine, and (iii) adenosine‐mediated vasoconstriction of the afferent arteriole.