Abstract

Adenosine 5′-triphosphate (ATP), when released from neuronal and non-neuronal tissues, interacts with cell surface receptors produces a broad range of physiological responses. The goal of the present study was to examine the issue of whether vascular smooth muscle cells respond to ATP. To this end, the dynamics of the intracellular concentration of calcium ions ([Ca 2+] i) in smooth muscle cells in testicular and cerebral arterioles was examined by laser scanning confocal microscopy. ATP produced an increase in [Ca 2+] i in arteriole smooth muscle cells. While P1 purinoceptor agonists had no effect on this process, P2 purinoceptor agonists induced a [Ca 2+] i increase and a P2 purinoceptor antagonist, suramin, completely inhibited ATP-induced [Ca 2+] i dynamics in both arteriole smooth muscle cells. In testicular arterioles, Ca 2+ channel blockers and the removal of extracellular Ca 2+, but not thapsigargin pretreatment, abolished the ATP-induced [Ca 2+] i dynamics. In contrast, Ca 2+ channel blockers and the removal of extracellular Ca 2+ did not completely inhibit ATP-induced [Ca 2+] i dynamics in cerebral arterioles. Uridine 5′-triphosphate caused an increase in [Ca 2+] i only in cerebral arterioles and α,β-methylene ATP caused an increase in [Ca 2+] i in both testicular and cerebral arterioles. We conclude that testicular arteriole smooth muscle cells respond to extracellular ATP via P2X purinoceptors and that cerebral arteriole smooth muscle cells respond via P2X and P2Y purinoceptors.

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