Second Messengers Are Involved in Facilitatory but Not Inhibitory Receptor Actions at Sympathetic Nerve Endings

Majewski, H.; Costa, Mônica Sarolli Silva de Mendonça; Foucart, Sylvain; Murphy, Timothy V.; Musgrave, Ian

doi:10.1111/j.1749-6632.1990.tb31999.x

Cited by 17 publications

(8 citation statements)

References 29 publications

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“…This pattern of effects was distinct from that observed upon activation of release enhancing b 2 -adrenoceptors, known to be coupled to G s -adenylate cyclase-protein kinase A pathway (Sibley and Lefkowitz 1987;Majewski et al 1990), or upon direct activation of adenylyl cyclase. a 2 -adrenoceptors, adenosine A 1 and P2Y receptors).…”

Section: Discussionmentioning

confidence: 74%

Adenosine A_2A receptor‐mediated facilitation of noradrenaline release involves protein kinase C activation and attenuation of presynaptic inhibitory receptor‐mediated effects in the rat vas deferens

Queiróz

Talaia

Gonçalves

2003

Journal of Neurochemistry

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In the epididymal portion of rat vas deferens, facilitation of noradrenaline release mediated by adenosine A2A receptors, but not that mediated by β2‐adrenoceptors or by direct activation of adenylyl cyclase, was attenuated by blockade of α2‐adrenoceptors and abolished by simultaneous blockade of α2‐adrenoceptors, adenosine A1 and P2Y receptors. The adenosine A2A receptor‐mediated facilitation was not changed by inhibitors of protein kinase A, protein kinase G or calmodulin kinase II but was prevented by inhibition of protein kinase C with chelerythrine or bisindolylmaleimide XI. Activation of protein kinase C with phorbol 12‐myristate 13‐acetate caused a facilitation of noradrenaline release that was abolished by bisindolylmaleimide XI and reduced by antagonists of α2‐adrenoceptors, adenosine A1 and P2Y receptors. Activation of adenosine A2A receptors attenuated the inhibition of noradrenaline release mediated by the presynaptic inhibitory receptors. This effect was mimicked by phorbol 12‐myristate 13‐acetate and prevented by bisindolylmaleimide XI. It is concluded that adenosine A2A receptors facilitate noradrenaline release by a mechanism that involves a protein kinase C‐mediated attenuation of effects mediated by presynaptic inhibitory receptors, namely α2‐adrenoceptors, adenosine A1 and P2Y receptors.

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Section: Discussionmentioning

confidence: 74%

Adenosine A_2A receptor‐mediated facilitation of noradrenaline release involves protein kinase C activation and attenuation of presynaptic inhibitory receptor‐mediated effects in the rat vas deferens

Queiróz

Talaia

Gonçalves

2003

Journal of Neurochemistry

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“…PKC is one of the intracellular effectors involved in the action of facilitatory prejunctional receptors of sympathetic nerve endings (Majewski et al, 1990). Indeed, the involvement of this protein kinase in the S-I release of NA has been shown in different experimental preparations, including rabbit hippocampus (Allgaier & Hertting, 1986), cat cerebral arteries (Balfagon et al, 1989), rat salivary gland (Wakade et al, 1985) and rat atria (Ishac & De Luca, 1988).…”

Section: Discussionmentioning

confidence: 99%

“…The intracellular effectors involved in the action of many facilitatory prejunctional receptors of peripheral sympathetic nerve terminals are either adenylate cyclase or protein kinase C (PKC) (Majewski et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

Modulatory effect of bradykinin on the release of noradrenaline from rat isolated atria

Chulak

Couture

Foucart

1995

British J Pharmacology

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4 The effect of BK was not affected by diclofenac (1 fiM), a cyclo-oxygenase inhibitor. Bisindolylmaleimide (1 gLM), a protein kinase C inhibitor, significantly reduced the facilitatory effect of BK (10 nM), angiotensin II (0.3 p4M) and phorbol dibutyrate (0.1 and 1 f1M) but not of fenoterol (1 fM). 5 The results suggest that BK enhances noradrenaline release via a prejunctional B2 kinin receptor in the rat atrium. The effect appears to involve protein kinase C as a second messenger.

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“…A dose-dependent facilitatory effect of cell-permeable cAMP analogues has been previously observed in mouse atria42 and the human pulmonary artery.43 It has been suggested that the facilitatory effect of f3-adrenergic receptor activation on norepinephrine release is linked to stimulation of adenylate cyclase and, hence, an increased formation of cAMP. 44 In the present study, a combination of 8-bromo-cAMP and the nonselective phosphodiesterase inhibitor IBMX45 was used to test this hypothesis. If intraneuronal levels of 8-bromo-cAMP and endogenous cAMP were already maximally increased, then isoproterenol should not be able to enhance neurotransmitter release through a cAMP-dependent mechanism.…”

Section: Camp and Norepinephrine Releasementioning

confidence: 98%

Beta 2-adrenergic receptor and angiotensin II receptor modulation of sympathetic neurotransmission in human atria.

Rump

Schwertfeger

Schaible

et al. 1994

Circulation Research

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The aim of the present study was to investigate beta-adrenergic receptor and angiotensin II (Ang II) receptor modulation of norepinephrine release in human atria. Slices of human atrial appendages were incubated with [3H]norepinephrine, superfused with Krebs-Henseleit solution, and electrically stimulated in superfusion chambers. Pretreatment of the tissue with 6-hydroxydopamine (1.2 mmol/L) before the [3H]norepinephrine incubation to destroy sympathetic nerves reduced the uptake of radioactivity and abolished the stimulation-induced (S-I) outflow of radioactivity. Furthermore, S-I outflow of radioactivity was prevented by the addition of tetrodotoxin (1 mumol/L) to and omission of extracellular Ca2+ from the superfusion solution. Separation of [3H]norepinephrine from its metabolites revealed that the S-I outflow of radioactivity was mainly composed of intact [3H]norepinephrine. Thus, the S-I outflow of radioactivity was taken as an index of norepinephrine release. Isoproterenol (0.001 to 0.1 mumol/L) dose-dependently enhanced the S-I outflow of radioactivity. The concentration-response curve of isoproterenol was shifted to the right by the selective beta 2-adrenergic receptor antagonist ICI 118551 (0.01 and 0.1 mumol/L) but not by the beta 1-adrenergic receptor-selective antagonist atenolol (0.3 and 30 mumol/L). Ang II (0.001 to 1.0 mumol/L) also dose-dependently enhanced S-I outflow of radioactivity. The facilitatory effect of Ang II was blocked by either the peptide Ang II receptor antagonist saralasin (1.0 mumol/L) or EXP 3174 (0.1 mumol/L), the in vitro active form of the nonpeptide Ang II receptor antagonist losartan. The cell-permeable cAMP analogue 8-bromo-cAMP (30 to 300 mumol/L) dose-dependently enhanced S-I outflow of radioactivity.(ABSTRACT TRUNCATED AT 250 WORDS)

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Second Messengers Are Involved in Facilitatory but Not Inhibitory Receptor Actions at Sympathetic Nerve Endings

Cited by 17 publications

References 29 publications

Adenosine A_2A receptor‐mediated facilitation of noradrenaline release involves protein kinase C activation and attenuation of presynaptic inhibitory receptor‐mediated effects in the rat vas deferens

Adenosine A_2A receptor‐mediated facilitation of noradrenaline release involves protein kinase C activation and attenuation of presynaptic inhibitory receptor‐mediated effects in the rat vas deferens

Modulatory effect of bradykinin on the release of noradrenaline from rat isolated atria

Beta 2-adrenergic receptor and angiotensin II receptor modulation of sympathetic neurotransmission in human atria.

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Second Messengers Are Involved in Facilitatory but Not Inhibitory Receptor Actions at Sympathetic Nerve Endings

Cited by 17 publications

References 29 publications

Adenosine A2A receptor‐mediated facilitation of noradrenaline release involves protein kinase C activation and attenuation of presynaptic inhibitory receptor‐mediated effects in the rat vas deferens

Adenosine A2A receptor‐mediated facilitation of noradrenaline release involves protein kinase C activation and attenuation of presynaptic inhibitory receptor‐mediated effects in the rat vas deferens

Modulatory effect of bradykinin on the release of noradrenaline from rat isolated atria

Beta 2-adrenergic receptor and angiotensin II receptor modulation of sympathetic neurotransmission in human atria.

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Adenosine A_2A receptor‐mediated facilitation of noradrenaline release involves protein kinase C activation and attenuation of presynaptic inhibitory receptor‐mediated effects in the rat vas deferens

Adenosine A_2A receptor‐mediated facilitation of noradrenaline release involves protein kinase C activation and attenuation of presynaptic inhibitory receptor‐mediated effects in the rat vas deferens