Regular ArticleAnti-adrenergic effect of adenosine on Na+–Ca2+exchange currentrecorded from guinea-pigventricular myocytes
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Mechanisms underpinning protection against eccentric exercise-induced muscle damage by ischemic preconditioning
2017, Medical HypothesesCitation Excerpt :It was previously shown that IPC of the cardiac muscle may lead to blunted ionic alterations [112,113] but the effects on skeletal muscle ionic handling are currently unknown. However, the circulating concentration of metabolic vasoactive autacoid adenosine is increased through IPC [114] and has been shown to prevent an excessive influx of Ca2+-ions via ATP-dependent K+-channels [115] and/or inhibition of NCX [116], induced by adenosine A1-receptors. Similar to muscle damage observed in I/R-Injury [87], EIMD is also likely to affect primarily fast-twitch rather than slow-twitch fibers [117].
Longstanding complex regional pain syndrome is associated with activating autoantibodies against alpha-1a adrenoceptors
2014, PainCitation Excerpt :In the whole CRPS group, results for baseline, transient, or ratio were not correlated with the patients’ disease durations (not shown); when setting a disease duration cutoff of 24 months, 4/6 patients with higher, and 6/12 patients with lower disease duration had tested positive. To try to define IgG-induced receptor activation, since baseline calcium is known to be under parasympathetic control [54], we assessed whether blockade of muscarinergic acetylcholine receptors with atropine would reverse the effect on this parameter. In 5 IgG preparations with marked effects on diastolic calcium, co-incubation with atropine partially normalized baseline calcium (average 60% normalization toward the healthy mean, Table 1), and also partially normalized the calcium transient (21% normalization), and ratio (29%).
β-Adrenoceptor/PKA-stimulation, Na<sup>+</sup>-Ca<sup>2+</sup> exchange and PKA-activated Cl<sup>-</sup> currents in rabbit cardiomyocytes: A conundrum
2011, Cell CalciumCitation Excerpt :Extracellular Ni2+ is used conventionally to measure INCX as it blocks both the inward and the outward INCX reliably and reversibly with no preference for either mode of transport [11–13]. Although it has been established that NCX1 can be phosphorylated by protein kinase A (PKA) and protein kinase C (PKC) at sites residing in the large intracellular loop of the NCX protein [16–18], functional regulation of mammalian NCX1 by the β-adrenoceptor/PKA pathway is controversial, with both reports of no alteration [19–24] or upregulation [2,14,15,25–27] of NCX activity in different studies. For example, previous work from this laboratory has provided evidence for an increase in guinea-pig ventricular NCX activity at 37 °C through the β-adrenoceptor/PKA pathway [14,15,25]: the currents recorded during voltage-ramps in NCX recording conditions were stimulated by the β-adrenoceptor agonist, isoprenaline (ISO), by the adenylyl cyclase activator, forskolin, or by raised [cAMP]i and the rate of decay of caffeine-induced [Ca2+]i transients were accelerated by high [cAMP]i [15].
Electrogenic Na<sup>+</sup>/Ca<sup>2+</sup>-exchange of nerve and muscle cells
2007, Progress in NeurobiologyIsoproterenol does not enhance Ca-dependent Na/Ca exchange current in intact rabbit ventricular myocytes
2005, Journal of Molecular and Cellular CardiologyCitation Excerpt :Schulze et al. [14] proposed that cardiac NCX is part of a regulatory macromolecular complex including PKA (analogous to the ryanodine receptor complex) [15], but evidence of direct NCX activation is mixed. Minor (25–100%) NCX enhancement with β-adrenergic stimulation was reported in intact cells [12,16,17], but not in subcellular preparations [6]. Recently, though, in contrast with all previous reports, a dramatic increase (up to fivefold) in NCX current with isoproterenol (ISO) was observed in Xenopus oocytes expressing rat cardiac NCX [12] and in native swine myocytes [18].
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Correspondence to: J. C. Hancox, Department of Physiology and Cardiovascular Research Laboratories, School of Medical Sciences, University Walk, Bristol BS8 1TD, UK. Tel.: +44 (0)1179289090; Fax: +44 (0)117929 3194; E-mail:[email protected]