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The effects of ATP and α,β‐methylene‐ATP on cytosolic Ca 2+ level and force in rat isolated aorta

1993; Wiley; Volume: 110; Issue: 1 Linguagem: Inglês

10.1111/j.1476-5381.1993.tb13803.x

1476-5381

Satoshi Kitajima, Hiroshi Ozaki, Hideaki Karaki,

Cardiac Ischemia and Reperfusion

The effects of a non‐selective P 2 ‐receptor agonist ATP and a selective P 2x ‐receptor agonist α,β‐methylene‐ATP on intracellular free Ca 2+ level ([Ca 2+ ] i ) and force were examined in rat isolated aorta without endothelium. Both ATP (1–1000 μ m ) and α,β‐methylene‐ATP (0.1–100 μ m ) induced transient increase followed by small sustained increase in [Ca 2+ ] i in a concentration‐dependent manner. Compared with the force induced by a high concentration of KCl, the force induced by α,β‐methylene‐ATP was smaller and that induced by ATP was much smaller at a given [Ca 2+ ] i . An L‐type Ca 2+ channel blocker, verapamil (10 μ m ), completely inhibited the high K + ‐stimulated [Ca 2+ ] i and force. Verapamil partially inhibited the transient and sustained increases in [Ca 2+ ] i induced by 10 μ m α,β‐methylene‐ATP and the sustained increase but not the transient increase induced by 1 m m ATP. In the absence of extracellular Ca 2+ (with 0.5 m m EGTA) 1 m m ATP caused transient increase in [Ca 2+ ] i while 10 μ m α,β‐methylene‐ATP was ineffective ATP, but not α,β‐methylene‐ATP, increased the tissue adenosine 3′:5′‐cyclic monophosphate (cyclic AMP) level. These data suggest that ATP and α,β‐methylene‐ATP increase [Ca 2+ ] i by an activation of both L‐type and non‐L‐type Ca 2+ channels. In addition, ATP, but not α,β‐methylene‐ATP, increases [Ca 2+ ] i by a release of Ca 2+ from an intracellular Ca 2+ store. Possible reasons are discussed as to why the increase in [Ca 2+ ] i due to ATP and α,β‐methylene‐ATP resulted in only a small contraction.