External ATP mimics carbachol in initiating calcium mobilization from pancreatic β‐cells conditioned by previous exposure to glucose

Abstract

1 Exposure to ATP (2-200 pM) resulted in a prominent peak of 45Ca efflux, when P-cell-rich pancreatic islets from ob/ob-mice were perifused with a Ca2+-deficient medium. ADP and the stable /x/p-methylene analogues of ATP and ADP also had stimulatory effects. 2 The nucleotide initiation of "5Ca efflux mimicked that obtained with carbachol both in requiring previous exposure to glucose and in being more pronounced after replacing extracellular Na+ by K+. 3 It was possible to induce repeated peaks of stimulated 45Ca efflux, when the exposure to ATP was interrupted with intervals of perifusion with glucose-containing media. 4 The observations are consistent with the existence of P2-purinoceptors in islets, suggesting that these receptors mediate a similar mobilization of calcium as noted when activating polyphosphoinositide breakdown with carbachol. In view of the high contents of ATP and ADP in the 13-cell secretory granules, activation of P2-purinoceptors should be considered as a possible mechanism for amplification of the initial insulin secretory response.

ATP‐induced Ca2+ release and Cl‐ current in cultured smooth muscle cells from pig aorta.

“…It can be observed that this substitution shifts the reversal potential to more positive potentials from a value of -5-5 mV in 100 % to + 1-2 mV in 50 % Cl-. The magnitude of this shift is close to the value of the shift of the equilibrium potential of Cl-ions by a 50 % reduction of (Benham, 1989b (Hallam & Pearson, 1986;Gylfe & Helman, 1987;McMillian, Soltoff, Cantley & Talamo, 1987;Phaneuf et al 1987;Tawada et al 1987;Fine, Cole & Davidson, 1989; Pearce, Murphy, Jeremy, Morrow & Dandona, 1989;Sasakawa, Nakaki, Yamamoto & Kato, 1989). It and in rabbit portal vein (Byrne & Large, 1988).…”

The effects of Bay K 8644 and nifedipine on the responses of rat urinary bladder to electrical field stimulation, β,γ‐methylene ATP and acetylcholine

“…In the dog mesenteric artery, nifedipine can selectively inhibit the purinergic component of the contractions evoked by sympathetic nerve stimulation (Omote et al, 1989), and in snail neurones nanomolar concentrations of extracellular ATP can activate membrane calcium channels (Yatani et al, 1982). Also, P2-purinoceptor-mediated calcium mobilization across the cell membrane has been observed in rat isolated alveolar type II cells (Dorn et al, 1989), murine thymocytes (El-Moatassim et al, 1989), human promyelocyteic cell line HL60 (Nonotte et al, 1989), Ehrlich ascites tumour cells (Dubyak & De Young, 1985), pancreatic i-cells (Gylfe & Hellman, 1987) and rat parotid acinar cells (McMillian et al, 1987).…”

Oscillatory control of insulin secretion

“…PLC activity was early detected in rodent islets (Schrey and Montague, 1983;Dunlop and Larkins, 1986), and subsequent analyses have demonstrated islet expression of several PLC-β, -γ, and -δ isozymes Zawalich et al, 1995;Gasa et al, 1999;Zawalich and Zawalich, 2000;Kim et al, 2001a;Kim et al, 2001b). The importance of PLC activity for insulin secretion is underlined by the fact that the enzyme is activated not only after exposure of islets and β-cells to various G-protein coupled receptor stimuli, such as acetylcholine/carbachol (Best and Malaisse, 1983;Hellman and Gylfe, 1986a;Best et al, 1987;Biden et al, 1987;Gilon and Henquin, 2001) and ATP (Gylfe and Hellman, 1987;Blachier and Malaisse, 1988), but also after exposure to glucose (Axen et al, 1983;Best and Malaisse, 1983;Laychock, 1983;Montague et al, 1985) and depolarizing agents (Laychock, 1983;Mathias et al, 1985;Best et al, 1987;Biden et al, 1987;Zawalich and Zawalich, 1988 (Prentki et al, 1988;Gylfe, 1991;Hellman et al, 1992;Theler et al, 1992;Miura et al, 1996) and these oscillations are characterized by a much shorter period than the glucose-induced, slow oscillations described above. Most of the [Ca 2+ ] i -elevating effect is due to IP 3 -mediated Ca 2+ mobilization from the ER, but the emptying of the stores also triggers Ca 2+ entry through store-operated channels in the plasma membrane (Liu and Gylfe, 1997;Miura et al, 1997;Dyachok and Gylfe, 2001).…”