Atp-induced cytosolic ca2+ rise involves different p2 receptor subtypes in freshly isolated and cultured aortic myocytes. Pacaud, Pierre, Rab[acute]e Malam-Souley, Gervaise Loirand, and Claude Desgranges. Laboratoire de Physiologie, Facult[acute]e de m[acute]edecine Victor Pachon, Universit[acute]e de Bordeaux II, Bordeaux ; INSERM U -390 H[circumflex]opital Arnaud de Villeneuve, Montpellier, and INSERM U-8 H[circumflex]opital Haut-L[acute]ev[circumflex]eque, Bordeaux, France
APStracts 2:0109H, 1995.
In vascular smooth muscle, extracellular ATP induces an increase in intracellular [Ca2+] ([Ca2+]i). Various agonists have been used to characterize P2 purinoceptor subtypes involved in the ATP-induced [Ca2+]i rise, measured by indo-1 fluorescence, in both freshly isolated and cultured rat aortic smooth muscle cells. [alpha],[beta] -methylene-ATP increased [Ca2+]i via Ca2+ entry through P2X receptor -channel in freshly isolated but not in cultured cells. 2-methylthio -ATP and ADP failed to release Ca2+ via P2Y receptor activation in freshly isolated cells whereas such a response was obtained in cultured cells. UTP, by stimulating P2U receptor, released Ca2+ from intracellular store in both freshly isolated and cultured cells. These results suggest that, in the course of the culture process, P2X receptor activation-induced responses were lost whereas P2Y receptor activation-induced [Ca2+]i rise appeared, these two phenomena being independent. Responses to P2X receptor agonist were lost whatever the culture conditions whereas functional P2Y receptors appeared only in cells that were stimulated with serum to induce cell cycle progression. The phenotypic modulation of vascular myocytes was therefore associated with a change in the functional P2 purinoceptor subtypes. 

Received 10 November 1994; accepted in final form 13 February
1995.
APS Manuscript Number H1002-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on  4 April 1995.