Cardiovascular effects of intracerebroven-tricular norepinephrine in conscious and anaesthetized monkeys

Forsyth, Ralph P.; Pesout, J

doi:10.1016/0028-3908(78)90121-1

Cited by 14 publications

(1 citation statement)

References 14 publications

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“…Consequently, further release induced by central stimulation would have little impact on the overall peptide concentration, resulting in reduced responses. Previous evidence pointed out that anesthesia may affect CNS‐mediated responses cardiovascular, such as those caused by intracerebroventricular (icv) NA or clonidine (Forsyth and Pesout, 1978; Corrêa et al, 1982). Also, anesthesia was reported to block the pressor responses caused by icv angiotensin II (Severs and Daniels‐Severs, 1973; Hoffman and Phillips, 1976).…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular effects of noradrenaline microinjection in the bed nucleus of the stria terminalis of the rat brain

Crestani

Alves

Resstel

et al. 2007

J of Neuroscience Research

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The bed nucleus of the stria terminalis (BST) is a limbic structure involved in regulating the hypothalamic-pituitary-adrenal axis as well as in central cardiovascular control. We report here on cardiovascular effects caused by microinjection of noradrenaline (NA) in the BST of the rat brain and the peripheral mechanisms involved in their mediation. Injection of NA (3, 7, 10, 15, 30, or 45 nmol in 100 nl) in the BST of unanesthetized rats caused long-lasting dose-related pressor and bradycardiac responses. No responses were observed when the dose of 10 nmol NA was microinjected into surrounding structures, such as the anterior commissure, the stria terminalis, the fornix, and the internal capsule, indicating a predominant action at the BST. Additionally, microinjection of 50 nmol tyramine, an indirectly acting sympathomimetic amine, caused similar pressor response, indicating local NA release in the BST. Responses to NA microinjection in the BST were markedly reduced in urethane-anesthetized rats, favoring the idea of a central action without significant leakage to the peripheral circulation. The pressor response was potentiated by i.v. pretreatment with the ganglion blocker pentolinium and blocked by i.v. pretreatment with the selective V(1)-vasopressin antagonist dTyr(CH(2))(5)(Me)AVP, suggesting its mediation by vasopressin release into circulation. The bradycardiac response to NA microinjected into the BST was also abolished by pretreatment with the vasopressin antagonist, indicating its reflex origin. In conclusion, results indicate that microinjection of NA into the BST evokes pressor responses, which are mediated by acute vasopressin release.

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Section: Discussionmentioning

confidence: 99%

Cardiovascular effects of noradrenaline microinjection in the bed nucleus of the stria terminalis of the rat brain

Crestani

Alves

Resstel

et al. 2007

J of Neuroscience Research

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The alpha2-adrenergic receptor system in the hypothalamus of the Pekin duck

Müller

Gerstberger

1992

Cell Tissue Res

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In the present study, we have employed the monoradioiodinated alpha 2-agonist clonidine ([125I]-CLO) to characterize duck hypothalamic alpha 2-adrenoceptors and to localize alpha 2-specific binding sites in the duck brain. To validate the alpha 2-specificity of [125I]-CLO using an enriched duck hypothalamic membrane fraction, a radioreceptor assay was established by altering the membrane protein concentration, time, temperature and ionic milieu of incubation, and in the presence or absence of protease inhibitors. Competitive displacement studies revealed the following sequence of potency to displace [125I]-CLO: yohimbine greater than (-)-epinephrine greater than clonidine greater than (-)-norepinephrine greater than phentolamine greater than (-)-phenylephrine greater than (-)-isoproterenol greater than prazosin. The non-hydrolyzable guanosine 5'-triphosphate analog guanylylimidodiphosphate markedly inhibited [125I]-CLO binding suggestive of G-protein involvement. With regard to the histological distribution, diencephalic structures, such as the habenula and the nucleus reticularis of the thalamus, were densely labeled by [125I]-CLO. In the hypothalamus, alpha 2-adrenoceptors were detected in the antidiuretic hormone-synthesizing nucleus paraventricularis, the nucleus praeopticus medialis, the nucleus anterior medialis hypothalami, the nucleus magnocellularis praeopticus, the nucleus commissurae pallii, the nucleus inferior hypothalami and the regio lateralis hypothalami. Circumventricular organs, such as the plexus choroidei, organum subfornicale, organum paraventriculare and the corpus pineale, were endowed with alpha 2-specific binding sites, as were the cell layers of the tectum opticum. In addition, telencephalic structures revealed high receptor densities.(ABSTRACT TRUNCATED AT 250 WORDS)

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Involvement of central dopamine receptors in the hypotensive action of pergolide

Jadhav

Willett

Sapru

et al. 1983

Naunyn-Schmiedeberg's Arch. Pharmacol.

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The involvement of central dopamine receptors in the hypotensive action of the dopaminergic ergoline, pergolide was determined in anesthetized rats. Intravenous (i.v.) or intracerebroventricular (i.v.t.) administration of pergolide (12.5, 25 and 50 micrograms/kg) produced dose-dependent decreases in blood pressure. The magnitude of hypotension seen following either i.v. or i.v.t. administration of pergolide was similar. However, while both sulpiride (1 mg/kg, i.v.) as well as phentolamine (1 mg/kg, i.v.) antagonized the hypotensive action of i.v. pergolide, only sulpiride (1 mg/kg, i.v.t.) was able to antagonize the hypotension seen following i.v.t. administration of pergolide. Phentolamine (1 mg/kg, i.v.t.) did not alter the central hypotensive action of pergolide. In a separate group of rats, clonidine (25 micrograms/kg, i.v.t.) also produced a decrease in blood pressure. While phentolamine (i.v.t.) antagonized the central hypotensive action of clonidine, sulpiride (i.v.t.) did not have any effect on the action of clonidine. These results show that selective activation of central dopamine receptors was responsible for the hypotensive action of centrally-administered pergolide. In a separate group of rats greater splanchnic sympathetic nerve activity was measured. Intravenous pergolide produced similar hypotensive response as seen in previous groups, and this was accompanied by a concomitant decrease in the sympathetic nerve activity. The maximum fall in blood pressure (26 +/- 6 mm Hg) was correlated with a 40% reduction in sympathetic nerve activity. The return of blood pressure to control levels occurred after 60-70 min and was also associated with the return of sympathetic nerve activity to control levels.(ABSTRACT TRUNCATED AT 250 WORDS)

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Cardiovascular effects of intracerebroven-tricular norepinephrine in conscious and anaesthetized monkeys

Cited by 14 publications

References 14 publications

Cardiovascular effects of noradrenaline microinjection in the bed nucleus of the stria terminalis of the rat brain

Cardiovascular effects of noradrenaline microinjection in the bed nucleus of the stria terminalis of the rat brain

The alpha2-adrenergic receptor system in the hypothalamus of the Pekin duck

Involvement of central dopamine receptors in the hypotensive action of pergolide

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