Platelet serotonin uptake during myocardial ischemia

Oei, H H; Hughes, William E.; Schaffer, Stephen W.; Longenecker, Gesina L.; Glenn, Thomas M.

doi:10.1016/0002-8703(83)90655-5

Cited by 11 publications

(10 citation statements)

References 10 publications

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“…Briefly, we believe that this method of evoking the CCR with increasing doses of PBG, which activate only a subset of CCR afferents, is a good, well controlled experimental tool widely accepted in the field (Cao and Morrison, 2000;Dias et al, 2005;Ditting et al, 2006;Veelken et al, 1993;Higuchi et al, 1988;Kashihara et al, 2003;Salo et al, 2007;Scislo and DiCarlo, 1994;Scislo et al, 1993). Selective activation of serotonin 5HT 3 receptors on polymodal vagal afferents from cardiopulmonary area dissects the activation of CCR from other reflexes and humoral mechanisms which may be triggered by cardiac ischemia which is known to naturally activate the CCR (Lupinski et al, 2011;Rocha et al, 2003;Schultz, 2001;Hainsworth, 1991;Burnstock et al, 1988;Oei et al, 1983). Although we could not distinguish between adrenal nerve fibers supplying adrenergic vs. noradrenergic chromafin cells in the adrenal medulla it has been shown previously that both these types of adrenal nerve fibers are similarly inhibited by activation of the CCR (Cao and Morrison, 2000).…”

Section: Discussionmentioning

confidence: 99%

Nucleus tractus solitarii A2a adenosine receptors inhibit cardiopulmonary chemoreflex control of sympathetic outputs

Minic¹,

O’Leary²,

Scislo³

2014

Autonomic Neuroscience

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Previously we have shown that stimulation of inhibitory A1 adenosine receptors located in the nucleus tractus solitarii (NTS) attenuates cardiopulmonary chemoreflex (CCR) evoked inhibition of renal, adrenal and lumbar sympathetic nerve activity and reflex decreases in arterial pressure and heart rate. Activation of facilitatory A2a adenosine receptors, which dominate over A1 receptors in the NTS, contrastingly alters baseline activity of regional sympathetic outputs: it decreases renal, increases adrenal and does not change lumbar nerve activity. Considering that NTS A2a receptors may facilitate release of inhibitory transmitters we hypothesized that A2a receptors will act in concert with A1 receptors differentially inhibiting regional sympathetic CCR responses (adrenal>lumbar>renal). In urethane/chloralose anesthetized rats (n=38) we compared regional sympathetic responses evoked by stimulation of the CCR with right atrial injections of serotonin 5HT3 receptor agonist, phenylbiguanide, (1–8 µg/kg) before and after selective stimulation, blockade or combined blockade and stimulation of NTS A2a adenosine receptors (microinjections into the NTS of CGS-21680 0.2–20 pmol/50 nl, ZM-241385 40 pmol/100 nl or ZM-241385+CGS-21680, respectively). We found that stimulation of A2a adenosine receptors uniformly inhibited the regional sympathetic and hemodynamic reflex responses and this effect was abolished by the selective blockade of NTS A2a receptors. This indicates that A2a receptor triggered inhibition of CCR responses and the contrasting shifts in baseline sympathetic activity are mediated via different mechanisms. These data implicate that stimulation of NTS A2a receptors triggers unknown inhibitory mechanism(s) which in turn inhibit transmission in the CCR pathway when adenosine is released into the NTS during severe hypotension.

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Section: Discussionmentioning

confidence: 99%

Nucleus tractus solitarii A2a adenosine receptors inhibit cardiopulmonary chemoreflex control of sympathetic outputs

Minic¹,

O’Leary²,

Scislo³

2014

Autonomic Neuroscience

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“…This reflex may be activated with serotonin (operating via 5HT 3 receptors) which is released during cardiac ischemia from aggregating platelets forming coronary thromboses, or from ischemic endothelial cells (Oei et al. ; Burnstock et al. ; Evans et al.…”

Section: Introductionmentioning

confidence: 99%

Colocalization of A_2abut not A₁adenosine receptors with GABA-ergic neurons in cardiopulmonary chemoreflex network in the caudal nucleus of the solitary tract

et al. 2018

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Adenosine operating in the nucleus of the solitary tract (NTS) may inhibit or facilitate neurotransmitter release from nerve terminals and directly inhibit or facilitate central neurons via A1 and A2a pre‐ and postsynaptic receptors, respectively. However, adenosine A2a receptors, may also activate GABA‐ergic neurons/terminals which in turn inhibit glutamatergic transmission in the NTS network. Our previous studies showed that adenosine operating via both A1 (inhibitor) and A2a (activator) receptors powerfully inhibits the cardiopulmonary chemoreflex (CCR) at the level of the caudal NTS. A1 receptors most likely inhibit glutamate release in the CCR network, whereas A2a receptors facilitate NTS GABA‐ergic mechanisms which in turn inhibit CCR glutamatergic transmission. Therefore, we hypothesized that A2a receptors are located on NTS GABA‐ergic neurons/terminals whereas A1 receptors may be located on NTS glutamatergic neurons/terminals. We investigated this hypothesis using double immunofluorescent staining for A2a or A1 adenosine receptors and GABA synthesizing enzyme, GAD67, in 30 μm thick, floating, medullary rat sections. We found that A2a adenosine receptors are localized within the GABA‐ergic cells in the caudal NTS, whereas A1 adenosine receptors are absent from these neurons. Instead, A1 receptors were located on non‐GABA‐ergic (likely glutamatergic) neurons/terminals in the caudal NTS. These data support our functional findings and the hypothesis that adenosine A2a, but not A1 receptors are located on GABA‐ergic neurons.

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“…The majority of cardiac vagal afferents activated by mechanical stimuli in the rat are also activated by the serotonin 5HT 3 receptor agonist phenylbiguanide (PBG) (51, 52). Cardiopulmonary chemoreflex may be naturally activated via serotonin released from aggregated platelets during coronary cloth formation or from ischemic endothelial cells (8,26,42) as well as via other naturally released substances' for example, endogenous canabinoids operating via activation of vanilloid TRPV1 receptors, ATP operating via P2x receptors, nicotine, etc. (25, 37, 47).…”

mentioning

confidence: 99%

Activation of NTS A₁adenosine receptors inhibits regional sympathetic responses evoked by activation of cardiopulmonary chemoreflex

Ichinose

Minic

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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Previously we have shown that adenosine operating via the A1receptor subtype may inhibit glutamatergic transmission in the baroreflex arc within the nucleus of the solitary tract (NTS) and differentially increase renal (RSNA), preganglionic adrenal (pre-ASNA), and lumbar (LSNA) sympathetic nerve activity (ASNA>RSNA≥LSNA). Since the cardiopulmonary chemoreflex and the arterial baroreflex are mediated via similar medullary pathways, and glutamate is a primary transmitter in both pathways, it is likely that adenosine operating via A1receptors in the NTS may differentially inhibit regional sympathetic responses evoked by activation of cardiopulmonary chemoreceptors. Therefore, in urethane-chloralose-anesthetized rats ( n = 37) we compared regional sympathoinhibition evoked by the cardiopulmonary chemoreflex (activated with right atrial injections of serotonin 5HT3receptor agonist phenylbiguanide, PBG, 1–8 μg/kg) before and after selective stimulation of NTS A1adenosine receptors [microinjections of N6-cyclopentyl adenosine (CPA), 0.033–330 pmol/50 nl]. Activation of cardiopulmonary chemoreceptors evoked differential, dose-dependent sympathoinhibition (RSNA>ASNA>LSNA), and decreases in arterial pressure and heart rate. These differential sympathetic responses were uniformly attenuated in dose-dependent manner by microinjections of CPA into the NTS. Volume control ( n = 11) and blockade of adenosine receptor subtypes in the NTS via 8-( p-sulfophenyl)theophylline (8-SPT, 1 nmol in 100 nl) ( n = 9) did not affect the reflex responses. We conclude that activation of NTS A1adenosine receptors uniformly inhibits neural and cardiovascular cardiopulmonary chemoreflex responses. A1adenosine receptors have no tonic modulatory effect on this reflex under normal conditions. However, when adenosine is released into the NTS (i.e., during stress or severe hypotension/ischemia), it may serve as negative feedback regulator for depressor and sympathoinhibitory reflexes integrated in the NTS.

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Platelet serotonin uptake during myocardial ischemia

Cited by 11 publications

References 10 publications

Nucleus tractus solitarii A2a adenosine receptors inhibit cardiopulmonary chemoreflex control of sympathetic outputs

Nucleus tractus solitarii A2a adenosine receptors inhibit cardiopulmonary chemoreflex control of sympathetic outputs

Colocalization of A_2abut not A₁adenosine receptors with GABA-ergic neurons in cardiopulmonary chemoreflex network in the caudal nucleus of the solitary tract

Activation of NTS A₁adenosine receptors inhibits regional sympathetic responses evoked by activation of cardiopulmonary chemoreflex

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Platelet serotonin uptake during myocardial ischemia

Cited by 11 publications

References 10 publications

Nucleus tractus solitarii A2a adenosine receptors inhibit cardiopulmonary chemoreflex control of sympathetic outputs

Nucleus tractus solitarii A2a adenosine receptors inhibit cardiopulmonary chemoreflex control of sympathetic outputs

Colocalization of A2abut not A1adenosine receptors with GABA-ergic neurons in cardiopulmonary chemoreflex network in the caudal nucleus of the solitary tract

Activation of NTS A1adenosine receptors inhibits regional sympathetic responses evoked by activation of cardiopulmonary chemoreflex

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Colocalization of A_2abut not A₁adenosine receptors with GABA-ergic neurons in cardiopulmonary chemoreflex network in the caudal nucleus of the solitary tract

Activation of NTS A₁adenosine receptors inhibits regional sympathetic responses evoked by activation of cardiopulmonary chemoreflex