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Invasive Hemodynamic Characterization of the Portal-hypertensive Syndrome in Cirrhotic Rats
Published on: August 1, 2018
Calcium-dependent diuretic system in preascitic liver cirrhosis
G Sansoè1, M Aragno, C E Tomasinelli
1Division of Gastroenterology, Gradenigo Hospital, Torino, Italy. giovannisan@iol.it
Journal of Hepatology
|August 27, 2010
Summary
In cirrhosis, reduced kidney calcium-sensing receptors (CaRs) cause sodium retention. A CaR agonist (PolyAg) normalized sodium excretion and improved kidney function in cirrhotic rats.
Area of Science:
- Nephrology
- Gastroenterology
- Pharmacology
Background:
- Extracellular calcium (Ca++) activates calcium-sensing receptors (CaRs) in renal tubules.
- CaR activation stimulates prostaglandin E(2) (PGE(2)) production, inhibiting sodium and water reabsorption.
- This system plays a role in regulating renal function.
Purpose of the Study:
- To investigate the function of the CaR-PGE(2) system in experimental cirrhosis.
- To assess the impact of a CaR-selective agonist (PolyAg) on renal function in cirrhotic rats.
Main Methods:
- CCl(4)-induced preascitic cirrhosis model in rats.
- Evaluation of renal function, hormonal status, urinary PGE(2) excretion.
- Measurement of renal CaR and Na(+)-K(+)-2Cl(-) co-transporter (BSC-1) protein levels via Western blot.
- Administration of PolyAg to assess its effects.
Main Results:
- Cirrhotic rats exhibited reduced urine volume and sodium excretion compared to controls.
- Kidneys of cirrhotic rats showed decreased CaR and increased BSC-1 protein expression.
- PolyAg treatment normalized urine and sodium excretion, increased renal plasma flow, PGE(2) excretion, and free-water clearance in cirrhotic rats.
Conclusions:
- Sodium retention in preascitic cirrhosis is associated with down-regulated renal CaRs and up-regulated sodium-retaining transporters.
- Calcimimetic drugs, like PolyAg, can normalize sodium retention in preascitic cirrhosis.
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