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Adenosine induces mesangial cell contraction by an A1-type receptor
A Olivera1, S Lamas, D Rodriguez-Puyol
1Medical Research Institute, Fundación Jiménez Diaz-Consejo Superior de Investigaciones Cientificas, Madrid, Spain.
Kidney International
|June 1, 1989
Summary
Adenosine causes kidney mesangial cells to contract by activating the A1 receptor, which requires calcium influx. This finding clarifies adenosine
Area of Science:
- Nephrology
- Cell Biology
- Pharmacology
Background:
- Adenosine is known to reduce renal blood flow and glomerular filtration rate.
- The specific effects of adenosine on mesangial cells and the underlying receptor mechanisms remain unclear.
Purpose of the Study:
- To investigate the hypothesis that adenosine induces contractile effects on mesangial cells.
- To identify the specific adenosine receptor subtype (A1 or A2) involved in this response.
- To determine the role of calcium in adenosine-mediated mesangial cell contraction.
Main Methods:
- Cultured rat mesangial cells were treated with varying concentrations of adenosine.
- Cell contraction was quantified by measuring changes in planar cell surface area (PCSA).
- Selective adenosine receptor agonists and antagonists, as well as verapamil and calcium-free conditions, were used to elucidate the mechanism.
Main Results:
- Adenosine induced a time- and dose-dependent reduction in PCSA, indicating mesangial cell contraction.
- The A1 receptor antagonist PD116,948 blocked adenosine-induced contraction, while the A2 antagonist PD115,199 did not.
- The A1 agonist S-PIA decreased PCSA, whereas the A2 agonist NECA did not.
- Verapamil and calcium-free medium prevented adenosine-induced contraction, highlighting the dependence on calcium influx.
Conclusions:
- Adenosine induces specific contraction of cultured rat mesangial cells.
- This contraction is primarily mediated by the adenosine A1 receptor.
- Extracellular calcium influx is essential for adenosine-induced mesangial cell contraction.