ArticleKidney & blood pressure research2008
Effect of adenosine on membrane potential and Ca2+ in juxtaglomerular cells. Comparison with angiotensin II.
Article in Kidney & blood pressure research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Adenosine inhibits renin release from juxtaglomerular cells via an A1 receptor-TRPC-mediated pathway.American journal of physiology. Renal physiology · 2013Article
- Regulation of renin secretion by renal juxtaglomerular cells.Pflugers Archiv : European journal of physiology · 2013Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
backgroundRenin is mainly secreted from the juxtaglomerular cells (JGC) in the kidney situated in the afferent arteriole close to the vessel pole. Angiotensin II (ANG II) and adenosine inhibit renin secretion and synergistically constrict the afferent arteriole. ANG II depolarises JGC and increases the cytoplasmic free Ca2+ concentration [Ca2+]i. The responses of JGC to adenosine are less known.
methodsEffects of adenosine on membrane potential and [Ca2+]i were studied in afferent arterioles from NaCl-depleted rats and mice.
resultStimulation of A1 adenosine receptors (A1AR) by adenosine (10 microM) or cyclohexyladenosine (1 microM) increased the spiking frequency of JGC, slightly depolarised the cells and, in < or =50% of the cases, increased [Ca2+]i. These effects were much smaller than those of ANG II (3 nM). Simultaneous application of cyclohexyladenosine and ANG II gave only additive effects on [Ca2+]i; in addition, responses to ANG II in JGC from A1AR knockout mice were similar to those from control mice.
conclusionThe small changes in membrane potential and [Ca2+]i in response to A1AR stimulation as compared to those of ANG II may suggest that these 2 tissue hormones use different signal transduction mechanisms to affect JGC function, including the inhibition of renin release.
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