α-MSH and other ACTH fragments improve cardiovascular function and survival in experimental hemorrhagic shock
References (64)
- et al.
Adrenal-independent, anti-shock effect of ACTH-(1–24) in rats
European J. Pharmacol.
(1986) - et al.
ACTH-(1–24) antagonizes the contractile effect of morphine on the isolated rat colon
European J. Pharmacol.
(1985) - et al.
ACTH-induced changes in the transmitteramine concentration of individual brain nuclei of the rat
- et al.
Cardiovascular effects of intravenous morphine in the anesthetized rat
European J. Pharmacol.
(1971) The opioid system and central cardiovascular control: analysis of controversies
Peptides
(1985)- et al.
Noradrenergic neurons: morphine inhibition of spontaneous activity
European J. Pharmacol.
(1974) - et al.
An effect of β-melanocyte stimulating hormone (β-MSH) on α-motoneurons of cat spinal cord
European J. Pharmacol.
(1977) - et al.
β-Endorphin and male sexual behavior
European J. Pharmacol.
(1977) - et al.
The turnover rate of acetylcholine in brain nuclei of rats injected intraventricularly and intraseptally with alpha and beta-endorphin
Neuropharmacology
(1978) - et al.
The effects of sodium chloride and calcium concentration on the response of melanophores to melanocyte-stimulating hormone (MSH)
Gen. Comp. Endocrinol.
(1962)
The opiomelanotropinergic neuronal and endocrine systems
Peptides
An inhibitory role of β-endorphin in central cardiovascular regulation
Life Sci.
Comparison of chronic and acute effects of morphine sulfate on cardiovascular function
Am. J. Cardiol.
Endorphin-mediated inhibition of locus coeruleus neurons
Brain Res.
Effect of beta-endorphin on the steroid production of isolated zona glomerulosa and zona fasciculata cells
Life Sci.
Corticotropin inhibits food intake in rats
Neuropeptides
Effects of two ACTH-analogs on noradrenaline metabolism in rat brain
Brain Res.
Interaction of peptides related-ACTH, MSH and β-LPH with neurotransmitters in the brain
Pharmacol. Ther.
Cardiovascular effects of peptides related to the enkephalins and β-casomorphin
Life Sci.
ACTH-like neurotropic peptides: possible regulators of rat brain cyclic AMP
Brain Res.
ACTH-like peptides and morphine: interaction at the level of the CNS
Psychoneuroendocrinology
Increase of hippocampal acetylcholine turnover rate and stretching-yawning syndrome elicited by alpha-MSH and ACTH
Life Sci.
Antagonism between morphine and the polypeptides ACTH, ACTH 1–24 and β-MSH in the nervous system
Immunocytochemical distribution of corticotropin (ACTH) in monkey brain
Neurology
Binding of 3H-β-endorphin to rat brain membranes: characterization of opiate properties and interaction with ACTH
European J. Pharmacol.
Opioids and neuropeptides: mechanisms in circulatory shock
Evidence and implications of a melanocortins-endorphins homeostatic system
Adrenocorticotropin reversal of experimental hemorrhagic shock is antagonized by morphine
Life Sci.
ACTH-induced hyperalgesia in rats
Experientia
Evidence that melanocortins are physiological antagonists of opioids
Induction of sexual excitement by the action of adrenocorticotrophic hormone in brain
Nature
Effects of ACTH-like neuropeptides on animal behavior and man
Pharmacology
Cited by (93)
Role of the brain melanocortins in blood pressure regulation
2017, Biochimica et Biophysica Acta - Molecular Basis of DiseaseCitation Excerpt :In addition, previous studies also showed that hemorrhagic shock reversal is mediated via CNS POMC-MC4Rs and may involve activation of efferent vagal cholinergic pathways [74]. For instance, microinjections of α-MSH in the nucleus ambiguus (nAMB) exerted excitatory effects on parasympathetic preganglionic neurons via activation of MC4R, resulting in increased vagal input to the heart and bradycardia responses [74–76]. These findings suggest that MC4R may play a role in mediating the parasympathetic component of baroreflex-induced bradycardia.
Centrally acting leptin induces a resuscitating effect in haemorrhagic shock in rats
2012, Regulatory PeptidesMelanocortins as potential therapeutic agents in severe hypoxic conditions
2012, Frontiers in NeuroendocrinologyCitation Excerpt :In these conditions, that in turn lead to the death of all saline-treated control animals within 30–35 min [15,16,18], conventional anti-shock drugs such as the glucocorticoid methylprednisolone, protease inhibitor aprotinin and sympathomimetic agent norepinephrine are ineffective [8]. Conversely, the intravenous bolus injection of nanomolar amounts of melanocortins [e.g., ACTH-(4–10), α-MSH, ACTH-(1–24), etc.] induces, within a few minutes, a dose-dependent restoration of arterial blood pressure and tissue blood flow, as well as a gradual normalization of blood gases, pH and lactate [12,15,16,18,89]. The melanocortin-induced shock reversal was found to be associated with a large increase in the volume of circulating blood, not due to hemodilution but as the consequence of the mobilization of the peripherally pooled residual blood that, in shock conditions, is trapped in capillaries and large blood reservoirs including liver and spleen [85,86,89].
Drug-induced activation of the nervous control of inflammation: A novel possibility for the treatment of hypoxic damage
2012, European Journal of PharmacologyCitation Excerpt :The minimum active dose [20 μg/kg in the case of ACTH-(1–24)] produces a 40% survival at 2 h after treatment; the maximum active dose (160 μg/kg) practically restores arterial pressure, pulse amplitude and respiratory rate to pre-bleeding values (Bertolini et al., 1986c), and produces a 100% survival – without reinfusion of the shed blood or infusion of blood substitutes – for more than 24 h (Bertolini et al., 1989). Adrenal glands are not involved, because the effect is the same either in intact or in adrenalectomized animals (Bertolini et al., 1986a) and is independent of the corticotropic activity of the melanocortin injected (Bertolini et al., 1986c). The resuscitating effect of melanocortins has been confirmed also in other shock conditions: the hypovolemic shock produced in rabbits by the graded occlusion of the inferior vena cava (Ludbrook and Ventura, 1995) and the rat model of splanchnic ischemia/reperfusion-induced shock (splanchnic artery occlusion shock, SAO shock) (Squadrito et al., 1999), and also in a pre-terminal condition produced in rats by prolonged asphyxia (Guarini et al., 1997).
Melanocortins counteract inflammatory and apoptotic responses to prolonged myocardial ischemia/reperfusion through a vagus nerve-mediated mechanism
2010, European Journal of PharmacologyBrain effects of melanocortins
2009, Pharmacological ResearchCitation Excerpt :In normotensive, normovolemic rats, either conscious or under light urethane anesthesia (a condition where cardiovascular reflexes and sufficient sympathetic tone are maintained), the intravenous injection of the adrenocorticotropin fragment ACTH4–10 and of γ1- and γ2-MSH (10 times more potent than ACTH4–10) induce a dose-dependent, short-lasting increase in blood pressure, heart rate and pulse amplitude, with a maximal effect 25 s following administration (for reviews see: [363–365]). Melanocortin peptides with a longer C-terminal extension, including γ3-MSH, α-MSH, ACTH1–17, ACTH1–24, and the whole 1–39 sequence of ACTH, are on the other hand devoid of these cardiovascular effects in the normotensive, normovolemic animal [68,199,366], but have dramatic and long-lasting cardiovascular effects in severe hypotensive conditions (for a review see: [76]). α-Melanocyte-stimulating hormone (α-MSH) is considered a trophic factor for nerve tissue, both during fetal development and in adulthood [5,148,447].