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

Abstract

Isolated rat ventricular cardiac myocytes loaded with the fluorescent calcium indicator fura2 Showed significant changes in intracellular calcium concentrations upon exposure to > 1/tM ATP (ECs0 = 7.4_ 1.3 gM, 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 #M norepinephrine decreased the concentration of ATP required for the Ca z ÷ transient, shifting the EC50 for ATP to 1.7 +_ 0.1 #M (n = 3, SE). fl-Propranolol (a ilrreceptor antagonist) prevented potentiation, whereas phentolamine (an ~q-receptor antagonist) did not, indicating that regulation is through the fll-adrenergic receptor. ATP and norepinephrine released locally from sympathetic neurons may act in concert through the ATP and fll-adrenergic receptors to regulate myocardial calcium homeostasis.

ATP and other adenine compounds increase mechanical activity and inositol trisphosphate production in rat heart.

“…More generally, ATP may be released simultaneously with noradrenaline or acetylcholine since several neurochemical studies suggest that single neurones may contain and release more than one active compound (Lundberg, Terenius, Hokfelt & Goldstein, 1983). Thus, ATP should be considered as a neurotransmitter in the mammal as well as in the frog heart (Hoyle & Burnstock, 1986) and may act in concert with other agonists to regulate myocardial calcium homeostasis (De Young & Scarpa, 1987).…”

Calcium antagonistic and antiarrhythmic actions of CPU‐23, a substituted tetrahydroisoquinoline

“…Measurements of [Ca2 li Ventricular myocytes were prepared from 200-250g male Sprague-Dawley rats according to the method described previously (Young & Scarpa, 1987;Huang & Wong, 1991) with slight modifications. In brief, the heart was mounted on a modified Langendorff perfusion apparatus and perfused at 10 ml min ' with oxygenated Joklik modified Eagles medium supplemented with 1.25 mM CaCI2 and 10 mM HEPES, pH 7.2, at 37C for 5 min followed by 5 min in the same medium without calcium.…”

Activation of chloride current by P2‐purinoceptors in rat ventricular myocytes

“…In the rat ventricular myocytes, previous reports show an increase in [Ca2+]i by an application of ATP (Danziger et'al., 1988;Bjornsson et al, 1989;de Young & Scarpa, 1987 ponses for both intracellular acidification (Puceat et al, 1991b) and extracellular phosphorylation (Christie et al, 1992) were observed at 60 s after the ATP application. Thus,…”