Facilitation of the release of noradrenaline: An extra-adrenal effect of adrenocorticotropic hormone

Szabó, Béla; Hedler, L; Starke, Klaus

doi:10.1016/0300-9572(89)90025-7

Cited by 13 publications

(19 citation statements)

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“…Other POMC-derived peptides, such as α-MSH, also facilitate noradrenaline release in the rabbit pulmonary artery, probably by activating the same presynaptic ACTH receptor (Göthert 1984). In pithed rabbits with electrically stimulated sympathetic outflow, ACTH-(1-24) dose-dependently (0.003-1 µg/kg min) decreased mean arterial pressure with no significant effect on heart rate (Szabo et al 1987(Szabo et al , 1989. There was an increase in plasma noradrenaline levels, but not in clearance, which suggested that the noradrenaline spillover rate reflected an increase in neuronal noradrenaline release as a result of activation of presynaptic ACTH receptors (Szabo et al 1989).…”

Section: Discussionmentioning

confidence: 99%

“…ACTH and ACTH-(1-24) enhance electrically stimulated neuronal noradrenaline release from isolated perfused rabbit hearts by postganglionic presynaptic ACTH receptors at concentrations as low as 100 pM (Szabo et al 1987(Szabo et al , 1989, and comparable ACTH-(1-24) concentrations inhibit tritiated noradrenaline uptake by spontaneously beating rat atria (Mehrabani and Bassett 1988). ACTH-(1-24) (0.1-100 nmol/l) increases the stimulus-evoked overflow of neuronal release of noradrenaline from isolated perfused rabbit hearts by postganglionic, presynaptic ACTH receptors (Szabo et al 1988(Szabo et al , 1989.…”

Section: Discussionmentioning

confidence: 99%

“…ACTH-(1-24) (0.1-100 nmol/l) increases the stimulus-evoked overflow of neuronal release of noradrenaline from isolated perfused rabbit hearts by postganglionic, presynaptic ACTH receptors (Szabo et al 1988(Szabo et al , 1989. ACTH-(1-24), but not α-MSH and ACTH-(4-10), enhance the myocardial sensitivity to noradrenaline in the electrically driven rat atrial strip preparation in a dose-dependent manner (Bassett et al 1978), probably by an inhibition of neuronal uptake by ACTH-(1-24) (Mehrabani and Bassett 1988).…”

Section: Discussionmentioning

confidence: 99%

“…Systemic administration of γ 2 -MSH to rats increases blood pressure, heart rate, and cerebral blood flow (Gruber and Callahan 1989;Sun et al 1992;De Wildt et al 1993Van Bergen et al 1995, 1996, 1997a. The structurally related peptide, ACTH-(1-24), appeared to be devoid of a pressor effect; rather it induces a depressor response in combination with a reflectory tachycardia in both anesthetized and conscious rats (Nakamura et al 1976;Van Bergen et al 1997a) and rabbits (Szabo et al 1989;Ludbrook and Ventura 1995).…”

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A study on possible modulating and direct effects of γ2-MSH and ACTH-(1–24) on the cardiovascular system of the rat

Bergen

Vleeming

Heijst

et al. 1998

Naunyn-Schmiedeberg's Arch Pharmacol

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In conscious rats, gamma2-melanocyte-stimulating hormone (gamma2-MSH) dose-dependently increases blood pressure and heart rate, whereas adrenocorticotropin-(1-24) [ACTH-(1-24)] dose-dependently decreases blood pressure, an effect which was accompanied by a reflectory tachycardia. As the exact mechanism involved in these cardiovascular effects of the two melanocortins is as yet not known, we undertook a series of experiments to investigate the possibility that these peptides have modulating or direct effect on the cardiovascular system of the rat. In pithed rats gamma2-MSH, administered intravenously (i.v.) in doses of 5-200 nmol/kg, had no significant effect on systolic and diastolic blood pressure and on heart rate, whereas ACTH-(1-24), 5-500 nmol/kg, i.v., dose-dependently decreased blood pressure and increased heart rate. Infusion of gamma2-MSH, 10(-8) M, or ACTH-(1-24), 10(-6) M, in the isolated perfused rat heart did not significantly affect left ventricular pressure or coronary flow. Pretreatment with either gamma2-MSH or ACTH-(1-24) did not modify the responsiveness of the myocardium and coronary vasculature to salbutamol and phenylephrine. Neither gamma2-MSH nor ACTH-(1-24) did affect the vascular contractile machinery of skinned vascular smooth muscles of the rabbit with respect to Ca2+ handling in the cell, as measured by its sensitivity to exogenously applied Ca2+. Gamma2-MSH had no effect on blood pressure and heart rate in pithed rats in which postganglionic sympathetic outflow was stimulated by 1,1-dimethyl-4-phenylpiperazinium (DMPP), nor in pithed rats in which preganglionic sympathetic outflow was stimulated electrically. A dose of 15 nmol/kg ACTH-(1-24) had no significant influence on preganglionic outflow to the cardiac and vascular structures in pithed rats. These data show that gamma2-MSH does not exert its cardiovascular effects via a peripheral site of action at the level of the vascular system and the heart, nor directly on pre- or postganglionic sympathetic outflow. These results are in support for the notion that the peptide acts via a brain region localised outside the blood-brain barrier. The acute depressor effect of ACTH-(1-24), however, seems to be due to a direct effect on the vasculature in the periphery.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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A study on possible modulating and direct effects of γ2-MSH and ACTH-(1–24) on the cardiovascular system of the rat

Bergen

Vleeming

Heijst

et al. 1998

Naunyn-Schmiedeberg's Arch Pharmacol

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“…Rather, it seems that melanocortins activate (or restore) a complex vasomotor reflex that eventually leads to the mobilization of the peripherally-pooled residual blood and which is seemingly obtunded, in conditions of failure of the circulatory homeostasis, by the massive release of endogenous opioids (Lang et al, 1982;Farrell et al, 1983;Holaday, 1983;Elam et al, 1984;Bernton et al, 1985;Schadt & Gaddis, 1985;Szabo et al, 1989;. Available data indicate that this vasomotor reflex involves afferent sensory fibres originating from vascular chemo-and baro-receptors, and efferent postganglionic sympathetic fibres.…”

Section: Introductionmentioning

confidence: 99%

Role of neuronal and vascular Ca²⁺‐channels in the ACTH‐induced reversal of haemorrhagic shock

Guarini

Bazzani

Bertolini

1993

British J Pharmacology

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Presynaptic Neuropeptide Receptors

Schlicker

Kathmann

2008

Handbook of Experimental Pharmacology

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Presynaptic receptors for four families of neuropeptides will be discussed: opioids, neuropeptide Y, adrenocorticotropic hormone (ACTH), and orexins. Presynaptic receptors for the opioids (micro, delta, kappa, and ORL(1)) and neuropeptide Y (Y(2)) inhibit transmitter release from a variety of neurones, both in the peripheral and central nervous systems. These receptors, which were also identified in human tissue, are coupled to G(i/o) proteins and block voltage-dependent Ca(2+) channels, activate voltage-dependent K(+) channels, and/or interfere with the vesicle release machinery. Presynaptic receptors for ACTH (MC(2) receptors) have so far been identified almost exclusively in cardiovascular tissues from rabbits, where they facilitate noradrenaline release; they are coupled to G(s) protein and act via stimulation of adenylyl cyclase. Presynaptic receptors for orexins (most probably OX(2) receptors) have so far almost exclusively been identified in the rat and mouse brain, where they facilitate the release of glutamate and gamma-aminobutyric acid (GABA); they are most probably linked to G(q) and directly activate the vesicle release machinery or act via a transduction mechanism upstream of the release process. Agonists and antagonists at opioid receptors owe at least part of their therapeutic effects to actions on presynaptic receptors. Therapeutic drugs targeting neuropeptide Y and orexin receptors and presynaptic ACTH receptors so far are not available.

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Facilitation of the release of noradrenaline: An extra-adrenal effect of adrenocorticotropic hormone

Cited by 13 publications

References 20 publications

A study on possible modulating and direct effects of γ2-MSH and ACTH-(1–24) on the cardiovascular system of the rat

A study on possible modulating and direct effects of γ2-MSH and ACTH-(1–24) on the cardiovascular system of the rat

Role of neuronal and vascular Ca²⁺‐channels in the ACTH‐induced reversal of haemorrhagic shock

Presynaptic Neuropeptide Receptors

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Facilitation of the release of noradrenaline: An extra-adrenal effect of adrenocorticotropic hormone

Cited by 13 publications

References 20 publications

A study on possible modulating and direct effects of γ2-MSH and ACTH-(1–24) on the cardiovascular system of the rat

A study on possible modulating and direct effects of γ2-MSH and ACTH-(1–24) on the cardiovascular system of the rat

Role of neuronal and vascular Ca2+‐channels in the ACTH‐induced reversal of haemorrhagic shock

Presynaptic Neuropeptide Receptors

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Role of neuronal and vascular Ca²⁺‐channels in the ACTH‐induced reversal of haemorrhagic shock