Cardiovascular responses of rats to intrahypothalamic injection of carbachol and noradrenaline

Poole, S.

doi:10.1111/j.1476-5381.1983.tb10006.x

Cited by 22 publications

(6 citation statements)

References 11 publications

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“…application of carbachol not only produced pressor responses in the nearterm ovine fetus but also increased the neural activity in the putative central cardiovascular controlling centers. The finding that c-fos expression was induced in the fetal AV3V and the hindbrain is the evidence that the central pathway are activated and cholinergic mechanisms are functional in the control of fetal blood pressure at 90% gestation, and indicates that the fetal AV3V region in the forebrain and In mature animals, carbachol is known as a long-lasting cholinergic agonist in the brain in affecting body fluid and cardiovascular homeostasis, including increase of arterial blood pressure, release of vasopressin, and stimulation of thirst (Barbosa et al, 1995;Iitake et al, 1986;Mahon et al, 1995;Poole, 1983). Previous studies in adults showed that the pressor response induced by central administered carbachol was marked and sustained with short latency (Poole, 1983;Ö zkutlu et al, 1994).…”

Section: Discussionmentioning

confidence: 94%

“…Central application of carbachol, a nonselective cholinergic agonist, produces an increase of blood pressure (BP), vasopressin release, and drinking (Barbosa et al, 1995;Iitake et al, 1986;Mahon et al, 1995;Poole, 1983). However, investigation of the development of brain cholinergic systems and their roles in cardiovascular homeostasis in utero has been very limited.…”

Section: Introductionmentioning

confidence: 99%

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The Association of Cardiovascular Responses with Brain c-fos Expression after Central Carbachol in the Near-Term Ovine Fetus

Shi

Morrissey

Yao

et al. 2005

Neuropsychopharmacol

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Central cholinergic mechanisms play important roles in the control of cardiovascular responses. However, in utero development of brain cholinergic mechanism in regulation of arterial pressure before birth is largely unknown. This study investigated cardiovascular responses to central application of carbachol in fetuses and determined functional development of the central cholinergic systems controlling fetal pressor responses in utero. Chronically prepared near-term ovine fetuses (90% gestation) received an injection of carbachol intracerebroventricularly (i.c.v.). Fetal cardiovascular responses were measured, and the brains were used for c-fos mapping studies. In response to carbachol injection i.c.v., fetal systolic, diastolic, and mean arterial pressure (MAP) immediately increased, accompanied by a bradycardia. The maximum increase of MAP was at 30 min after the i.c.v. injection of carbachol and lasted 90 min. Associated with the pressor response, the neuronal activity marked with c-fos was enhanced significantly in the fetal anterior third ventricle (AV3V) region (including the median preoptic nucleus and organum vasculosum of the lamina terminalis) in the forebrain, and in the area postrema, lateral parabrachial nucleus, nucleus tractus solitary, and rostral ventrolateral medulla in the hindbrain. These results indicate that the central cholinergic mechanism is functional in the control of fetal blood pressure at the last third of gestation, and the central AV3V region and hindbrain have been intact relatively during in utero development in sheep at 90% gestational stage.

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Section: Discussionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

The Association of Cardiovascular Responses with Brain c-fos Expression after Central Carbachol in the Near-Term Ovine Fetus

Shi

Morrissey

Yao

et al. 2005

Neuropsychopharmacol

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“…Direct injection of norepinephrine, epinephrine and clonidine into the AHA results in dose-related decreases in blood pressure and heart rate in rats [33][34][35]. Furthermore, in spontaneously hypertensive rats, hypertension induced by a high NaCl diet is associated with a reduced norepinephrine release in the AHA [17,36,37].…”

Section: Discussionmentioning

confidence: 99%

Direct Corticosteroid Modulation of GABAergic Neurons in the Anterior Hypothalamic Area of GAD65-eGFP Mice

Shin¹,

Han²,

Lee³

et al. 2011

Korean J Physiol Pharmacol

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Corticosterone is known to modulate GABAergic synaptic transmission in the hypothalamic paraventricular nucleus. However, the underlying receptor mechanisms are largely unknown. In the anterior hypothalamic area (AHA), the sympathoinhibitory center that project GABAergic neurons onto the PVN, we examined the expression of glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) of GABAergic neurons using intact GAD65-eGFP transgenic mice, and the effects of corticosterone on the burst firing using adrenalectomized transgenic mice. GR or MR immunoreactivity was detected from the subpopulations of GABAergic neurons in the AHA. The AHA GABAergic neurons expressed mRNA of GR (42%), MR (38%) or both (8%). In addition, in brain slices incubated with corticosterone together with RU486 (MR-dominant group), the proportion of neurons showing a burst firing pattern was significantly higher than those in the slices incubated with vehicle, corticosterone, or corticosterone with spironolactone (GR-dominant group; 64 vs. 11∼ 14% , p＜ 0.01 by χ 2 -test). Taken together, the results show that the corticosteroid receptors are expressed on the GABAergic neurons in the AHA, and can mediate the corticosteroid-induced plasticity in the firing pattern of these neurons. This study newly provides the experimental evidence for the direct glucocorticoid modulation of GABAergic neurons in the AHA in the vicinity of the PVN.

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“…In support of this hypothesis, Poole reported that the microinjection of NA into POA in rats increases arterial pressure. 24 The POA receives major noradrenergic innervation from the locus coeruleus (LC) and the other cell groups in the medula oblongata and pons. Noradrenergic neurons in the LC are strongly activated during recovery from halothane anesthesia.…”

Section: Discussionmentioning

confidence: 99%

Increased noradrenaline release from rat preoptic area during and after sevoflurane and isoflurane anesthesia

Anzawa

Kushikata

Ohkawa

et al. 2001

Can J Anesth/J Can Anesth

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Purpose: To study the effects of sevoflurane and isoflurane on noradrenaline release from the rat preoptic area (POA).Method: Sixteen male Wistar rats were studied. A microdialysis probe with a 2 mm long semipermeable membrane was implanted in the POA. Dialysates were collected at intervals often minutes. After obtaining five control samples for 50 rain, 30 rain inhalation of 3% sevoflurane or 1.8% isoflurane was performed. After cessation of the inhalation, five more samples were obtained for 50 rain as recovery phase. Noradrenaline (NA) concentration in the dialysates was measured by high pressure liquid chromatography with an electrochemical detector.Results: Both sevoflurane and isoflurane caused marked increases in NA release from the rat POA (sevoflurane 233% at 20 rain, isoflurane 357% at ten minutes after the start of inhalation). The marked NA releases were also observed during the emergence from sevoflurane and isoflurane anesthesia (sevoflurane 269% at 20 rain, isoflurane 368% at ten minutes in the recovery phase).Conclusion: This study suggests that enhanced release of NA in the POA during sevoflurane and isoflurane may explain the excitatory phase observed during the peri-anesthetic period with these agents. Objectif : Etudier les effets du s&oflurane et de I'isoflurane sur la lib&ation de noradr4naline en provenance de I'aire pr4optique du rat (APO). M~tbode

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Cardiovascular responses of rats to intrahypothalamic injection of carbachol and noradrenaline

Cited by 22 publications

References 11 publications

The Association of Cardiovascular Responses with Brain c-fos Expression after Central Carbachol in the Near-Term Ovine Fetus

The Association of Cardiovascular Responses with Brain c-fos Expression after Central Carbachol in the Near-Term Ovine Fetus

Direct Corticosteroid Modulation of GABAergic Neurons in the Anterior Hypothalamic Area of GAD65-eGFP Mice

Increased noradrenaline release from rat preoptic area during and after sevoflurane and isoflurane anesthesia

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