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Acta Physiologica Congress

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Acta Physiologica 2011; Volume 203, Supplement 688
The 62nd National Congress of the Italian Physiological Society
9/25/2011-9/27/2011
Sorrento, Italy


PURINERGIC RECEPTORS AND REGULATORY VOLUME DECREASE IN SEABREAM (SPARUS AURATA) HEPATOCYTES
Abstract number: P41

TORRE1 A, FEDELE1 G, TRISCHITTA1 F, FAGGIO1 C

1Dept Life Science, Univ. of Messina, Italy

The maintenance of a constant volume in anisosmotic condition is a homeostatic requirement in animal cells. Hepatocytes constantly undergo osmotic stress as a consequence of solute movements and metabolism. In euryhaline fish a further challenge to the maintenance of cell volume is the fact that transfer from seawater to freshwater or vice versa causes a transient haemodilution or haemoconcentration. Our previous studies showed that the seabream isolated hepatocytes exposed to a rapid change (from 370 to 260 mOsm/kg) of the osmolarity of the bathing solution swelled but thereafter exhibited a regulatory volume decrease (RVD) leading to a partial recovery of initial volume.

The aim of this work was to investigate whether the release of ATP from the cell is involved in the RVD response, as suggested for other cell types. Videometric methods were employed. The observation that apyrase, an ATP scavenger, strongly inhibited RVD in isolated seabream hepatocytes, suggests that extracellular ATP is a mediator of this homeostatic response. It is conceivable that the nucleotide stimulates RVD by interacting with P2 receptors, since in the presence of the agonist ATPgS the recovery of cell volume after the swelling produced by the hypotonic stress was more rapid and pronounced than in the control conditions; on the contrary RVD was inhibited by the P2 receptor antagonist, suramine. The observation that the P1 antagonist, 8PT, produced a complete recovery of cell volume, while the agonist adenosine inhibits the homeostatic response suggests that adenosine, produced by the dephosphorylation of extracellular ATP, interacts with P1 receptor and inhibits RVD.

To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 203, Supplement 688 :P41

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