Cardiac Noradrenaline Release Accelerates Adenosine Formation in the Ischemic Rat Heart: Role of Neuronal Noradrenaline Carrier and Adrenergic Receptors

Richardt, Gert; Blessing, Reinhard; Schömig, Albert

doi:10.1006/jmcc.1994.1150

Cited by 21 publications

(10 citation statements)

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“…These findings are consistent with those reported by Richardt et al, 28 which showed that only the time course, but not the total amount, of NA-induced ADO release was affected by ␤-adrenoceptor antagonism. The finding that atenolol had no effect on the CPT-induced increases in plasma ADO levels clearly ruled out ␤1-adrenoceptor activation as a mechanism responsible for the sympathetic stimulation-dependent production of ADO during CPT.…”

Section: Discussionsupporting

confidence: 93%

“…The finding that atenolol had no effect on the CPT-induced increases in plasma ADO levels clearly ruled out ␤1-adrenoceptor activation as a mechanism responsible for the sympathetic stimulation-dependent production of ADO during CPT. These findings are consistent with those reported by Richardt et al, 28 which showed that only the time course, but not the total amount, of NA-induced ADO release was affected by ␤-adrenoceptor antagonism.…”

Section: Discussionsupporting

confidence: 93%

“…7,[20][21][22][23] This reflex is elicited in the course of locally provoked ischaemia in the forearm, 4,5,7,24 leading to the release of noradrenaline (NA) 7,24 with an increase in arterial blood pressure and heart rate. In fact, an increase in venous plasma levels of ADO is observed following intracoronary infusion of NA 28,29 or during sympathetic nerve stimulation of the heart, 25,30 probably originating from dephosphorylation of ATP cosecreted with NA from adrenergic nerve endings. Indeed, the increase in the sympathetic tone affects, in turn, ADO formation.…”

Section: Introductionmentioning

confidence: 99%

“…Indeed, the increase in the sympathetic tone affects, in turn, ADO formation. In fact, an increase in venous plasma levels of ADO is observed following intracoronary infusion of NA 28,29 or during sympathetic nerve stimulation of the heart, 25,30 probably originating from dephosphorylation of ATP cosecreted with NA from adrenergic nerve endings. 27,31 On the basis of such premises, during provoked local ischaemia, ADO may originate either directly from the ischaemic tissue as an expression of metabolic changes or as a consequence of sympathetic system excitation.…”

Section: Introductionmentioning

confidence: 99%

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Systemic Adenosine Increase During Cold Pressor Test Is Dependent on Sympathetic Activation

Laghi-Pasini

Capecchi

Colafati³

et al. 1999

Clin Exp Pharma Physio

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1. Following local vasoconstriction-inducing stimuli, such as the cold pressor test (CPT), significant changes occur in haemodynamics, with a rise in arterial blood pressure and heart rate (HR) due to the activation of the sympathetic nervous system. Among the compensatory mechanisms to local ischaemia, the endogenous nucleoside adenosine (ADO) has been suggested to play a relevant role by contributing to sympathetic stimulation. The possibility was investigated that CPT-induced increases in plasma ADO levels were not only an expression of the increased production of ADO in the ischaemic area, but also a consequence of systemic sympathoexcitatory mechanisms, thus showing a bidirectional involvement of the mechanisms of ADO formation. 2. The CPT was performed in 15 volunteers and mean arterial blood pressure (MABP) and HR were evaluated, together with plasma levels of noradrenaline (NA) and ADO in the tested and contralateral arm. The 15 subjects were then divided into three groups of five that were treated with either 5 mg transdermal clonidine weekly, 100 mg atenolol daily or 600 mg aminophylline twice daily. After 1 week treatment, the same test was repeated in the respective groups. 3. The CPT induced a rise in MABP and HR and an increase in plasma levels of NA and ADO. Increases in ADO were more pronounced in the tested arm. Clonidine blunted the haemodynamic response and NA release, while increases in ADO increase were reduced to a greater extent in the contralateral arm rather than the tested arm. Atenolol only affected MABP and HR without any effect on NA and ADO levels. Theophylline did not show any effect on CPT-induced changes. 4. In conclusion, local vasoconstriction and ischaemia induced in one arm following CPT are associated with haemodynamic changes dependent on the activation of the sympathetic system. The observed increase in plasma levels of ADO seems to be, in part, a direct expression of local responses to ischaemia (pre-dominant in the tested arm), but also appears as the consequence of systemic sympathoexcitatory mechanisms. Such increases in ADO are not dependent on a beta 1-adrenoceptor-mediated mechanism. Finally, theophylline, at a therapeutic dose, has no effect on the response to CPT.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Systemic Adenosine Increase During Cold Pressor Test Is Dependent on Sympathetic Activation

Laghi-Pasini

Capecchi

Colafati³

et al. 1999

Clin Exp Pharma Physio

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“…Although normally responsible for reuptake of noradrenaline, the neuronal catecholamine transporter has been shown to be responsible for nonexocytotic release of noradrenaline from sympathetic nerve terminals during ischemia. Increased release of noradrenaline has been implicated in ischemia-induced arrhythmia (63)(64)(65). Nandrolone has been shown to cause the release of intracellular calcium in rat primary myotubes, in a manner independent of intracellular androgen receptors but dependent on inositol triphosphate and the extracellular signal-regulated kinase pathway (66).…”

Section: Discussionmentioning

confidence: 99%

Nandrolone plus moderate exercise increases the susceptibility to lethal arrhythmias

Joukar¹,

Baravati²,

Fathpour³

et al. 2015

Res Cardiovasc Med

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Background: Until now, no experimental study has directly assessed the arrhythmogenesis of chronic consumption of anabolic androgenic steroids along with moderate-intensity endurance exercise. Objectives: We evaluated the influence of integration of anabolic androgenic steroids along with moderate-intensity endurance exercise on susceptibility to lethal ventricular arrhythmias in rat. Materials and Methods:The animal groups were as follows: control group (CTL); exercise group (EX) which were under 6 weeks of treadmill exercise; nandrolone group (Nan) which received 5 mg/kg of nandrolone decanoate twice a week; vehicle group (Arach) which received Arachis oil (solvent of nandrolone); trained vehicle group (Arach + Ex); and trained nandrolone group (Nan + Ex). One day after ending of the intervention period, arrhythmia was inducted by intravenous infusion of aconitine and ventricular arrhythmias were recorded. Then malondialdehyde (MDA) and glutathione peroxidase (GPX) of heart tissue were measured. Results: Nandrolone, exercise, and their combination were associated with heart hypertrophy. Exercise could prevent the incremental effect of nandrolone on MDA/GPX ratio. Chronic administration of nandrolone with moderate-intensity endurance exercise had no significant effect on blood pressure, heart rate, and basal electrocardiographic parameters. Combination of nandrolone and exercise significantly increased the incidence of ventricular fibrillation (VF) and reduced the VF latency (P < 0.05). Conclusions:The findings suggest that chronic coadministration of nandrolone with moderate-intensity endurance exercise facilitates the VF occurrence in rat. Complementary studies are needed to elucidate the involved mechanisms of this abnormality.

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Analysis of membrane transport mechanisms of endogenous substrates using chromatographic techniques

Yamaguchi

Mano

2019

Biomedical Chromatography

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Membrane transporters are expressed in various bodily tissues and play essential roles in the homeostasis of endogenous substances and the absortion, distribution and/or excretion of xenobiotics. For transporter assays, radioisotope-labeled compounds have been mainly used. However, commercially available radioisotopelabeled compounds are limited in number and relatively expensive. Chromatographic analyses such as high-performance liquid chromatography with ultraviolet absorptiometry and liquid chromatography with tandem mass spectrometry have also been applied for transport assays. To elucidate the transport properties of endogenous substrates, although there is no difficulty in performing assays using radioisotope-labeled probes, the endogenous background and the metabolism of the compound after its translocation across cell membranes must be considered when the intact compound is assayed. In this review, the current state of knowledge about the transport of endogenous substrates via membrane transporters as determined by chromatographic techniques is summarized. Chromatographic techniques have contributed to our understanding of the transport of endogenous substances including amino acids, catecholamines, bile acids, prostanoids and uremic toxins via membrane transporters.

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Cardiac Noradrenaline Release Accelerates Adenosine Formation in the Ischemic Rat Heart: Role of Neuronal Noradrenaline Carrier and Adrenergic Receptors

Cited by 21 publications

References 0 publications

Systemic Adenosine Increase During Cold Pressor Test Is Dependent on Sympathetic Activation

Systemic Adenosine Increase During Cold Pressor Test Is Dependent on Sympathetic Activation

Nandrolone plus moderate exercise increases the susceptibility to lethal arrhythmias

Analysis of membrane transport mechanisms of endogenous substrates using chromatographic techniques

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