Mechanism of the Differential Effects of Halothane on Nicotinic-and Muscarinic-Receptor-Mediated Responses of the Dog Adrenal Medulla

The effects of inhalation anesthetics on calcium-stimulated exocytosis in a natural membrane model system

“…However, in the presence of excess calcium, each of the examined anesthetics inhibited exocytosis to some extent. These results are generally consistent with prior studies showing that volatile anesthetics inhibit secretory processes in intact cells (Pocock and Richards, 1986;Cheek et al, 1986;Sumikawa et al, 1985;Bosnjak et al, 1982;Gothert et al, 1976) and provide experimental support for our hypothesis that halothane inhibits the formation of the echinoderm fertilization envelope by impairing the Ca2+-regulated fusion of cortical vesicles with the egg plasma membrane (Hinkley and Wright, 1986). Although our 9-10) at 22 ° .…”

“…These observations, in conjunction with the present data, suggest that exocytotic events in intact cells are more sensitive to anesthetics than those of isolated membrane (cortex) preparations. Supporting this notion, clinical concentrations of halothane have been reported to inhibit secretory events in intact chromaffin cells of the adrenal medulla (Pocock and Richards, 1986;Sumikawa et al, 1985;Gothert et al, 1976), mast cells in organ culture (Cheek at al., 1986), and explanted sympathetic ganglia (Bosnjak et al, 1982). A plausible explanation for the differences in anesthetic sensitivity observed between intact sea urchin eggs and isolated cortices is that volatile anesthetics may inhibit exocytosis by affecting some regulatory component or pathway (see below) which is partially inactivated or perhaps not well preserved in isolated cortices.…”

“…Studies in which the products secreted by intact cells have been measured generally support the conclusion that volatile anesthetics inhibit the fusion of secretory vesicles with the plasma membrane of a variety of cell types including chromaffin cells (Pocock and Richards, 1986;Sumikawa et al, 1985;Gothert et al, 1976), mast cells (Cheek at al., 1986), and even sympathetic neurons (Bosnjak et al, 1982). Paradoxically, recent studies clearly show that inhalati0nal anesthetics actually enhance the.…”

General anesthetic modulation of neuronal nicotinic acetylcholine receptors

“…The receptors in the presynaptic and preterminal regions, when activated, cause release of various transmitters including glutamate, GABA, ACh, dopamine and norepinephrine [2,3,5]. Inhalational anesthetics were indeed shown to suppress nicotine-induced dopamine release in rat striatum [12], nicotine-induced catecholamine release in chromaffin cells [11,14], and ACh release in rat striatum and cerebral cortex [13]. Our recent study also demonstrated that isoflurane and sevoflurane suppressed the release of glutamate and GABA in rat cortical neurons [9].…”

Inhibitory effects of propofol on catecholamine secretion and uptake in cultured bovine adrenal medullary cells

“…Recently, Lingen et al (1994) have cloned, expressed and pharmacologically characterized the noradrenaline transporter from the bovine adrenal medulla. Since ion channel-mediated catecholamine secretion and antidepressant-sensitive noradrenaline uptake have been well studied in the adrenal medullary cells, this preparation is a good tool for detailed analysis of the action of anaesthetics on the sympathetic nervous system (Sumikawa et al 1980(Sumikawa et al , 1982(Sumikawa et al ,1985Takara et al 1986;Yashima et al 1986;Richards 1988, 1991;Minami et al 1994). …”