Presynaptic ?2-adrenoceptor, opioid ?-receptor and adenosine A1-receptor interactions on noradrenaline release in rabbit brain cortex

Limberger, N.; Späth, L.; Starke, Klaus

doi:10.1007/bf00168812

Cited by 69 publications

(34 citation statements)

References 22 publications

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“…Similar results were also observed in the hamster mesenteric arterial bed, where the application of DPCPX had no effect on contractile responses elicited by electrical field stimulation [136]. It has been described that activation of presynaptic α 2 -adrenoceptors reduces the inhibitory effect on noradrenaline release of A 1 -receptor activation [4,15,91]. It is possible that, in splanchnic vascular beds, the adenosine inhibitory effect on transmitter release is revealed when presynaptic α 2 -adrenoceptors are blocked, as previously observed in other tissues [58,61,84].…”

Section: Adenosine Receptors In the Splanchnic Circulationsupporting

confidence: 77%

Purinergic receptors in the splanchnic circulation

Morato

Sousa

Albino‐Teixeira

2008

Purinergic Signalling

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There is considerable evidence that purines are vasoactive molecules involved in the regulation of blood flow. Adenosine is a well known vasodilator that also acts as a modulator of the response to other vasoactive substances. Adenosine exerts its effects by interacting with adenosine receptors. These are metabotropic G-protein coupled receptors and include four subtypes, A 1 , A 2A , A 2B and A 3 . Adenosine triphosphate (ATP) is a co-transmitter in vascular neuroeffector junctions and is known to activate two distinct types of P2 receptors, P2X (ionotropic) and P2Y (metabotropic). ATP can exert either vasoconstrictive or vasorelaxant effects, depending on the P2 receptor subtype involved. Splanchnic vascular beds are of particular interest, as they receive a large fraction of the cardiac output. This review focus on purinergic receptors role in the splanchnic vasomotor control. Here, we give an overview on the distribution and diversity of effects of purinergic receptors in splanchnic vessels. Pre-and post-junctional receptormediated responses are summarized. Attention is also given to the interactions between purinergic receptors and other receptors in the splanchnic circulation.

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Section: Adenosine Receptors In the Splanchnic Circulationsupporting

confidence: 77%

Purinergic receptors in the splanchnic circulation

Morato

Sousa

Albino‐Teixeira

2008

Purinergic Signalling

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“…Thus, overflow of noradrenaline evoked by electrical stimulation can be interpreted as noradrenaline release. cx2-Adrenoceptors were also blocked, so any interference of auto-inhibition mediated by prejunctional 2-autoreceptors with the effect of purinoceptor agonists and antagonists was avoided (see Enero & Saidman, 1977;Allgaier et al, 1987;Limberger et al, 1988;Guimaraes et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

Purinoceptor modulation of noradrenaline release in rat tail artery: tonic modulation mediated by inhibitory P_2Y‐ and facilitatory A_2A‐purinoceptors

Gonçalves

Queiróz

1996

British J Pharmacology

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1 The effects of analogues of adenosine and ATP on noradrenaline release elicited by electrical stimulation (5 Hz, 2700 pulses) were studied in superfused preparations of rat tail artery. The effects of purinoceptor antagonists, of adenosine deaminase and of adenosine uptake blockade were also examined. Noradrenaline was measured by h.p.l.c. electrochemical detection. 2 The A,-adenosine receptor agonist, N6-cyclopentyladenosine (CPA; 0.1-100 nM) reduced, whereas the A2A-receptor agonist 2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamidoadenosine (CGS 21680; 3-30 nM) increased evoked noradrenaline overflow. These effects were antagonized by the Aladenosine receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; 20 nM) and the A2-adenosine receptor antagonist, 3,7-dimethyl-1-propargylxanthine (DMPX; 100 nM), respectively. The P2Y-purinoceptor agonist, 2-methylthio-ATP (1-100 gM) reduced noradrenaline overflow, an effect prevented by the P2-purinoceptor antagonist, cibacron blue 3GA (100 gM) and suramin (100 gM).3 Adenosine deaminase (2 u ml-1), DMPX (100 nM) and inhibition of adenosine uptake with S-(pnitrobenzyl)-6-thioinosine (NBTI; 50 nM) decreased evoked noradrenaline overflow. DPCPX alone did not change noradrenaline overflow but prevented the inhibition caused by NBTI. The P2Y-purinoceptor antagonist, cibacron blue 3GA (100 gM) increased evoked noradrenaline overflow as did suramin, a nonselective P2-antagonist.4 It is concluded that, in rat tail artery, inhibitory (Al and P2y) and facilitatory (A2A) purinoceptors are present and modulate noradrenaline release evoked by electrical stimulation. Endogenous purines tonically modulate noradrenaline release through activation of inhibitory P2y and facilitatory A2A purinoceptors, whereas a tonic activation of inhibitory Al purinoceptors seems to be prevented by adenosine uptake.

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“…They might result from (i) the use of non-selective receptor ligands affecting more than one presynaptic receptor (ii) differences in the biophase concentration of NA so that a given partial agonist at a2-adrenoceptors could either facilitate or inhibit release, or (iii) a functional interaction between various presynaptic receptors (e.g. Limberger et al, 1988;Allgaier et al, 1989; 1991a; Molderings & Gbthert, 1990). …”

Section: Introductionmentioning

confidence: 99%

Effects of 5‐HT receptor agonists on depolarization‐induced [³H]‐noradrenaline release in rabbit hippocampus and human neocortex

Allgaier¹,

Warnke

Stangl³

et al. 1995

British J Pharmacology

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1 The present study attempted to determine whether noradrenaline (NA) NA release were investigated. 3 In rabbit hippocampus, 5-HT, 5-carboxamidotryptamine (5-CT; 32 pM) and 2-CH3-5-HT (32 pM) increased [3H]-NA release elicited with 360 pulses/3 Hz. Facilitation of transmitter release was not influenced by the 5-HT3 receptor antagonist, tropisetron but was prevented by the a2-adrenoceptor antagonist, rauwolscine. When autoinhibition was avoided by stimulating the tissue with 4 pulses/100 Hz (pseudo-one pulse-(POP) stimulation), 2-CH3-5-HT decreased evoked transmitter release, whereas 5-HT and 5-CT had no effect. Inhibition caused by 2-CH3-5-HT was not affected by tropisetron but counteracted by the x2-adrenoceptor ligands, clonidine and rauwolscine. Inhibition caused by clonidine was diminished in the presence of 5-CT or 2-CH3-5-HT.4 In human neocortex, [3H]-NA release elicited with 360 pulses/3 Hz was increased by 10 pM 5-HT and 32 pM 5-CT, whereas 2-CH3-5-HT was ineffective.[31H]-NA release evoked with a modified POP stimulation (2 bursts of 4 pulses/100 Hz, 3.5 min apart) was not affected by 2-CH3-5-HT or 5-CT. 5 The present results indicate that 5-HT, 2-CH3-5-HT and 5-CT can act on presynaptic a2-autoreceptors as partial agonists (2-CH3-5-HT; in rabbit hippocampal tissue) or antagonists (5-HT and 5-CT; in tissue of rabbit hippocampus and human neocortex). Furthermore the existence of autoinhibition dictates whether these drugs cause facilitation of release, inhibition or have no effect.

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Presynaptic ?2-adrenoceptor, opioid ?-receptor and adenosine A1-receptor interactions on noradrenaline release in rabbit brain cortex

Cited by 69 publications

References 22 publications

Purinergic receptors in the splanchnic circulation

Purinergic receptors in the splanchnic circulation

Purinoceptor modulation of noradrenaline release in rat tail artery: tonic modulation mediated by inhibitory P_2Y‐ and facilitatory A_2A‐purinoceptors

Effects of 5‐HT receptor agonists on depolarization‐induced [³H]‐noradrenaline release in rabbit hippocampus and human neocortex

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Presynaptic ?2-adrenoceptor, opioid ?-receptor and adenosine A1-receptor interactions on noradrenaline release in rabbit brain cortex

Cited by 69 publications

References 22 publications

Purinergic receptors in the splanchnic circulation

Purinergic receptors in the splanchnic circulation

Purinoceptor modulation of noradrenaline release in rat tail artery: tonic modulation mediated by inhibitory P2Y‐ and facilitatory A2A‐purinoceptors

Effects of 5‐HT receptor agonists on depolarization‐induced [3H]‐noradrenaline release in rabbit hippocampus and human neocortex

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Purinoceptor modulation of noradrenaline release in rat tail artery: tonic modulation mediated by inhibitory P_2Y‐ and facilitatory A_2A‐purinoceptors

Effects of 5‐HT receptor agonists on depolarization‐induced [³H]‐noradrenaline release in rabbit hippocampus and human neocortex