Extracellular ATP induces Ca2+ transients in cardiac myocytes which are potentiated by norepinephrine

FEBS Letters

Scarpa, Antonio¹  De Young, Mary Beth¹ 

[1] Department of Physiology and Biophysics, 2119 Abington Rd, Case Western Reserve University, Cleveland, OH 44106, USA

关键词: Myocyte;    ATP;    Norepinephrine;    Ca2+ transient;    Fura2;    BSA;    bovine serum albumin;    ITP;    inosine 5′-triphosphate;    UTP;    uridine 5′-triphosphate;    AMP-PNP;    5′-adenylyl imidophosphate;    ATPγS;    adenosine 5′-O-(3-thiotriphosphate);   

DOI  :  10.1016/0014-5793(87)80508-2

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Isolated rat ventricular cardiac myocytes loaded with the fluorescent calcium indicator fura2 showed significant changes in intracellular calcium concentrations upon exposure to > 1 μM ATP (EC₅₀ = 7.4 ± 1.3 μM, n = 4, SE), suggesting that extracellular ATP may have an important influence on myocardial contractility. The response was found to be highly ATP specific and required extracellular calcium. Furthermore, 30 s pretreatment of the cells with 0.2–1 μM norepinephrine decreased the concentration of ATP required for the Ca²⁺ transient, shifting the EC₅₀ for ATP to 1.7 ± 0.1 μM (n = 3, SE). β-Propranolol (a β₁-receptor antagonist) prevented potentiation, whereas phentolamine (an α₁-receptor antagonist) did not, indicating that regulation is through the β₁-adrenergic receptor. ATP and norepinephrine released locally from sympathetic neurons may act in concert through the ATP and β₁-adrenergic receptors to regulate myocardial calcium homeostasis.

【 授权许可】

Unknown