Response to ATP is accompanied by a Ca2+ influx via P2X purinoceptors in the coronary arterioles of golden hamsters

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  • Matsuura Makoto
    Department of Cell Biology and Neuroanatomy, Iwate Medical University
  • Saino Tomoyuki
    Department of Cell Biology and Neuroanatomy, Iwate Medical University
  • Satoh Yoh-ichi
    Department of Cell Biology and Neuroanatomy, Iwate Medical University

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Abstract

In the vascular wall, adenosine-5’-triphosphate (ATP) released along with noradrenaline from sympathetic nerve terminals is considered to play an important role in controlling intracellular calcium ion ([Ca2+] i) levels in arteries. The present study examined how vascular smooth muscle cells in coronary arterioles respond to ATP in relation to [Ca2+] i dynamics. For this purpose, the dynamics of [Ca2+] i in the coronary arterioles of golden hamsters was examined by real-time laser scanning confocal microscopy. This technique enabled the visualization of [Ca2+] i changes in response to ATP in the intact coronary arterioles, the ultrastructure of which was well preserved. It was shown that an increase in [Ca2+] i in the arteriole smooth muscle cells was elicited by ATP. While P1 purinoceptor agonists have no effect on this process, P2 purinoceptor agonists were found to induce a [Ca2+] i increase in the smooth muscle cells. Suramin (an antagonist of P2X and P2Y receptors) completely inhibited ATP-induced [Ca2+] i dynamics, but reactive blue 2 (a P2Y receptor antagonist) did not. Uridine-5’-triphosphate (a P2Y receptor agonist) had no effect on [Ca2+] i, but α,β- methylene ATP (a P2X receptor agonist) caused a strong increase in [Ca2+] i. We conclude that smooth muscle cells of the hamster coronary arterioles possess P2X, but not P1 or P2Y purinoceptors. The smooth muscle cells probably respond to extracellular ATP via P2X purinoceptors, resulting in the contraction of the coronary arterioles.

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