Effect of intraventricular administration of noradrenaline and dopamine on the levels of corticosterone in rats and denervation hypersensitivity resulting from intraventricular administration of 6-hydroxydopamine.

Kawa, A.; Taniguchi, Yoshiyasu; Mizuguchi, Katsumi; Ryu, Seiichiro; Ariyama, T.; Kamisaki, Takeshi; Koreeda, F.; Kanehisa, Takuya

doi:10.1016/0024-3205(78)90227-8

Cited by 25 publications

(19 citation statements)

References 12 publications

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“…Thus, drugs that do not cross the blood-brain bar rier in significant amounts, such as epinephrine [61] and norepinephrine [62,63], will not have this action whereas the more lipophilic methoxamine will. In support of our in terpretation is the finding that increased corticosteroid se cretion is seen in cats only after implantation of norepi nephrine into hypothalamic areas but not into the pituitary gland [32], Intracerebroventricular administration of nor epinephrine stimulates corticosteroid secretion in rats [1,29] but inhibits it in dogs [56]. The differences may be attri butable to the species or to the effects of drugs at more than one site following intracerebroventricular administration as opposed to hypothalamic implantation.…”

Section: Discussionmentioning

confidence: 50%

Alpha-Adrenergic Stimulation of Corticotropin Secretion by a Specific Central Mechanism in Man

et al. 1987

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In a double-blind study in normal subjects, methoxamine, a highly selective agonist at alpha-1-adrenoceptors, significantly increased circulating ACTH and cortisol. The stimulant effect of methoxamine on cortisol secretion was dose dependent in the range 3.5–7 µg/kg/min, was abolished by concomitant administration of the strong alpha-1-adrenergic (and weak HI) antagonist thymoxamine but unaffected by the antihistamine, chlorpheniramine. In order to test whether the action of methoxamine on ACTH secretion was exerted centrally or peripherally, the effects of norepinephrine (NE), an alpha-1-agonist that does not cross the blood-brain barrier, were studied. Doses of NE (1–12 µg/min) that increased systolic blood pressure by amounts similar to the changes produced by methoxamine, did not result in any rise in plasma cortisol in normal subjects. The effect of methoxamine, which is more lipid soluble than NE, on plasma ACTH and cortisol, appears to be exerted on the CNS and not at the pituitary or via nonspecific peripheral mechanisms. In addition to its water solubility, NE differs from methoxamine in its beta-1-, beta-2- and alpha-2-agonist actions. However, prenalterol (2 mg) and salbutamol (250 µg), respectively beta-1- and beta-2-adrenergic agonist drugs, had no effect on the secretion of ACTH or cortisol and the alpha-2-antagonist yohimbine in an effective dose did not unmask a stimulant effect of intravenous NE on plasma cortisol. At high infusion rates, NE significantly inhibited cortisol secretion. Stimulation of central alpha-1-adrenergic mechanisms results in secretion of ACTH in man, presumably by increased release of a corticotropin-releasing factor.

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Section: Discussionmentioning

confidence: 50%

Alpha-Adrenergic Stimulation of Corticotropin Secretion by a Specific Central Mechanism in Man

et al. 1987

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“…Nor epinephrine also inhibits the production of CRF by the rat hypothalamus in vitro [2]. However, norepinephrine has been reported to increase the plasma corticosterone concen tration similarly in stressed and intact rats [18].…”

Section: Discussionmentioning

confidence: 99%

The Effect of Adrenergic and Cholinergic Antagonists on Central Histaminergic Stimulation of Pituitary-Adrenocortical Response under Stress in Rats

Bugajski¹,

Gadek²

1984

Neuroendocrinology

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A possible interaction of central histaminergic receptors with adrenergic and cholinergic muscarinic neurons in increasing the pituitary-adrenocortical response under stress, assessed indirectly from the corticosterone concentration in blood serum, was investigated in conscious rats. All the drugs were administered intracerebroventriculary, the antagonists 15 to 30 min prior to the agonists. The histamine-induced increase in serum corticosterone levels of stressed rats was considerably antagonized by prazosin, phenoxybenzamine, phentolamine and yohimbine, α₁ and α₂-adrenergic antagonists. These antagonists abolished or significantly attenuated the corticosterone response to 2-pyridylethylamine (PEA), an H₁-receptor agonist, and to dimaprit and 4-methylhistamine(4-MeHA), H₂-receptor agonists. Propranolol, a β-adrenergic blocker, did not substantially change the corticosterone response induced by histamine or histamine H₁- and H₂-receptor agonists. Similarly, atropine was ineffective in blocking the increase in serum corticosterone responses induced by either histamine or PEA and dimaprit in stressed rats. These results suggest that both α₁- and α₂-adrenergic receptors, but not β-adrenergic and cholinergic muscarinic receptors interact with central H₁ and H₂ histaminergic stimulation of the increased pituitary-adrenocortical response in stressed rats.

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“…Activation of catecholaminergic pro jections during stress was indicated by the release of nor adrenaline (NA) in PVN by stressful stimuli [14][15][16], Moreover, specific lesioning of the CA innervation of the PVN significantly reduced the surge of CRF, ACTH and/ or corticosterone after various stressors [17][18][19][20][21][22][23]. In addi tion, NA or NA agonists, when injected intracerebroventricularly or locally into the PVN, have been shown to stimulate the release of ACTH [24][25][26][27][28][29] and CRF [27,30], The latter effects were blocked by a r antagonists [27,28,30]. Taken together, this evidence strongly suggested that the ascending catecholaminergic pathways originating from lower brainstem and projecting to the PVN may stimulate CRF-containing cells through a|-adrenoceptors and thus be involved in the activation of the HPA axis in response to stress.…”

Section: Introductionmentioning

confidence: 99%

Evidence that Activation of the Hypothalamo-Pituitary-Adrenal Axis by Electrical Stimulation of the Noradrenergic A1 Group Is Not Mediated by Noradrenaline

Gartside

Suaud-Chagny²,

Tappaz³

1995

Neuroendocrinology

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The paraventricular nucleus (PVN) of the hypothalamus, where the CRF-containing neurosecretory cells controlling the hypothalamo-pituitary-adrenal (HPA) axis are located, receives a dense noradrenergic innervation from the A1 group of the caudal ventrolateral medulla. In the present study we studied the relationship between release of noradrenaline (NA) in the PVN and activation of the HPA axis in response to electrical stimulation of the A1 region. In the urethane-anesthetized male rat, extracellular NA in the PVN was monitored on line by electrochemical recording while the activity of the HPA axis was estimated by measurement of ACTH in blood samples. A 1 min, 10 Hz stimulation evoked a significant increase of extracellular NA in the PVN as well as an ACTH surge in blood. The NA and ACTH response evoked by stimulation in the 3- to 14-Hz range were found to be frequency dependent. However, whilst the NA response increased in an exponential manner with respect to frequency, the ACTH response appeared to plateau between 10 and 14 Hz. Specific lesions of the noradrenergic terminals in the PVN, by bilateral local administration of 6-hydroxydopamine, markedly reduced the ACTH response to stimulation. Intracerebroventricular injection of desmethylimipramine, a NA uptake inhibitor, enhanced the increase in extracellular NA evoked by submaximal stimulation about 2.5-fold but did not modify the corresponding ACTH response. Combined intracerebroventricular injection of α-and β-adrenergic antagonists, phentolamine and propanolol respectively, did not prevent the ACTH response evoked by stimulation. Following stimulation of the caudal ventrolateral medulla, the ACTH response thus appears to result from the stimulation of the Al noradrenergic group projecting to the PVN. However, the inability of pharmacological manipulations which enhance or block central noradrenergic transmission to influence the ACTH response suggests that the noradrenergic endings in the PVN originating from the A1 group use a transmitter other than NA to activate the HPA axis at the PVN level.

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Effect of intraventricular administration of noradrenaline and dopamine on the levels of corticosterone in rats and denervation hypersensitivity resulting from intraventricular administration of 6-hydroxydopamine.

Cited by 25 publications

References 12 publications

Alpha-Adrenergic Stimulation of Corticotropin Secretion by a Specific Central Mechanism in Man

Alpha-Adrenergic Stimulation of Corticotropin Secretion by a Specific Central Mechanism in Man

The Effect of Adrenergic and Cholinergic Antagonists on Central Histaminergic Stimulation of Pituitary-Adrenocortical Response under Stress in Rats

Evidence that Activation of the Hypothalamo-Pituitary-Adrenal Axis by Electrical Stimulation of the Noradrenergic A1 Group Is Not Mediated by Noradrenaline

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