Intracranial injections of 6-hydroxydopamine (6-OH-DA) in cats: effects on the release of antidiuretic hormone

Milton, A. S.; Paterson, Anna T.

doi:10.1016/0006-8993(73)90550-7

Cited by 11 publications

(5 citation statements)

References 13 publications

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“…Recently, there has been increasing evidence that dopamine plays an important role in the control of AVP secretion. In vivo studies with cats show that injection of dopamine into the third ventricle or the nucleus accumbens will stimulate AVP secretion, whilst intracerebroventricular 6-hydroxy dopamine which depletes central monoaminergic neurones abolishes the AVP releasing effect of hypertonic saline (Milton & Paterson, 1973). Injection of dopamine into the supraoptic nucleus of the cat inhibits spontaneous firing, however, (Barker et al, 1971) and a diuretic effect has been recorded following injection into the third ventricle (Wolny et al, 1974).…”

Section: Discussionmentioning

confidence: 99%

“…These results suggest that dopamine inhibits the release of vasopressin, either by an action at pituitary level or at the median eminence of the hypothalamus.The neuropharmacological control of arginine vasopressin (AVP) release has been the subject of considerable controversy. Recent work has suggested an important role for dopamine in the control of AVP release in experimental animals (Milton 8c Paterson, 1973;Wolny et al, 1974;Bridges et al, 1976), although there is disagreement whether its effect is stimulatory or inhibitory. In humans there is also confusion with reports that some dopamine blocking agents increase AVP secretion (Shah et al, 1973;De Rivera, 1975), whilst others have been found to have no effect (Kendler et al, 1978).The present study was designed to test the effect of L-Dopa, a dopamine precursor, on resting levels of AVP, and the rise of AVP stimulated by head-up tilt (Davies et al, 1976; Bayliss 8t Heath, 1977).…”

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confidence: 99%

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Evidence for Dopamine as an Inhibitor of Vasoprotein Release in Man

Lightman

Forsling

1980

Clinical Endocrinology

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The effect of dopamine on vasopressin release was studied by the infusion of L-Dopa, a dopamine precursor that crosses the blood-brain barrier. L-Dopa suppressed resting levels of vasopressin and inhibited the rise of vasopressin produced by head-up tilt. Carbidopa, a decarboxylase inhibitor that does not cross the blood-brain barrier blocked the action of L-Dopa. These results suggest that dopamine inhibits the release of vasopressin, either by an action at pituitary level or at the median eminence of the hypothalamus.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Evidence for Dopamine as an Inhibitor of Vasoprotein Release in Man

Lightman

Forsling

1980

Clinical Endocrinology

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“…There is a close anatomic proximity of the centers regulating thirst (lateral hypothalamus, preoptic area, septum) and ADH release (SON), and these hypothalamic nuclei are interconnected with the limbic system. Dopamine regulates ADH release and extracellular stimulation of thirst, and the destruction of hypothalamic dopaminergic pathways abolished central receptor-induced ADH release in cats (Milton and Paterson, 1973) and produced adipsia in rats (Ungerstedt, 1971). However, a potential role of antipsychotic drug binding to sigma receptors in the supraoptic nucleus should be considered in the etiology of this syndrome.…”

Section: Table I Densities and Standard Errors Of Sigma Binding Sitmentioning

confidence: 99%

Sigma receptors are associated with cortical limbic areas in the primate brain

Mash

Zabetian

1992

Synapse

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Putative sigma receptors are a current target for antipsychotic drug development. Novel antipsychotic agents which possess selective and high affinity for sigma binding sites may serve as an alternative to the principal neuroleptic drugs currently in clinical use which mediate extrapyramidal side effects and dyskinesias through their blockade of dopamine receptors. We have used in vitro autoradiography to localize putative sigma receptors labelled with (+)-[3H]-3-(3-hydroxyphenyl)-N-(1-propyl)piperidine [(+)-[3H]-3-PPP] in the brain of the rhesus macaque. The binding characteristics of (+)-[3H]-3-PPP in the primate brain were comparable to those previously described in the rodent. Saturation analysis demonstrated a single class of sites in cerebellar and hippocampal membranes with a Kd value of 28 nM. Sigma receptors labeled with (+)-[3H]-3-PPP in the primate brain displayed the appropriate rank order of potency and stereoselectivity in competition binding assays. Haloperidol displaced (+)-[3H]-3-PPP binding in the low nanomolar range, and the (+) isomer of pentazocine was 50-fold more potent than (-) pentazocine. Computerized densitometric analysis of the autoradiograms demonstrated a striking enrichment of sigma binding sites over the paralimbic belt cortices, including the orbitofrontal, cingulate, insular, parahippocampal, and temporopolar gyri. Peak densities of sigma receptors were seen over the medial and central nuclei of the amygdala and were widely distributed within the hippocampal formation. Sigma binding sites densities were elevated over the suprachiasmatic and supraoptic nuclei of the hypothalamus. Moderate sigma receptor densities were observed over the ventromedial sectors of the caudate and the putamen. Sigma receptors were also elevated over autonomic relay nuclei of the brainstem, including the nucleus of the solitary tract and the dorsal motor nucleus of the vagus. The distribution of sigma receptors in the primate brain suggests that the paralimbic belt cortices, amygdala, hippocampus, hypothalamus, and autonomic relay nuclei of the brainstem may be interrelated by a topographic chemical linkage. The autoradiographic visualization of sigma receptor distributions in the primate brain provides further support for a role of sigma receptor mechanisms in the functions of the limbic system.

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“…Equally controversial is the notion of dopaminergic control of AVP release. Animal studies disagree as to whether this is a stimulatory or inhibitory effect or whether it exists at all (Milton & Paterson, 1973;Wolny et al, 1974;Bridges et al, 1976;Cadnapaphornchai et al, 1977;Ball et al, 1981;Hatzinikolaou et al, 1984). Studies in man are equally contradictory, some reporting an inhibitory effect (Shah et al, 1973;De Correspondence: Dr J. J. Morton, MRC Blood Pressure Unit, Western Infirmary, Glasgow GI 1 6NT, UK.…”

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confidence: 99%

The Role of Plasma Osmolality, Angiotensin Ii and Dopamine in Vasopressin Release in Man

Morton

Connell

Hughes

et al. 1985

Clinical Endocrinology

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A sensitive and specific radioimmunoassay for arginine vasopressin was used to compare the relative importance of changes in plasma osmolality, angiotensin II and dopamine in the regulation of vasopressin secretion in man. One hour after water loading plasma vasopressin fell from 0.40 to 0.06 pmol/l, while 8 h and 24 h fluid restriction resulted in a rise of vasopressin from 0.29 to 0.54 and 1.37 pmol/l respectively. In contrast neither dietary sodium deprivation, when plasma angiotensin II increased 5-fold, nor dopamine infusion, at a rate which increased circulating dopamine levels up to 244-fold, had any effect on basal plasma vasopressin values. These results confirm that, under physiological conditions, osmoregulation is the major mechanism controlling vasopressin release and suggests that circulating angiotensin II and dopamine have no significant part to play.

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Intracranial injections of 6-hydroxydopamine (6-OH-DA) in cats: effects on the release of antidiuretic hormone

Cited by 11 publications

References 13 publications

Evidence for Dopamine as an Inhibitor of Vasoprotein Release in Man

Evidence for Dopamine as an Inhibitor of Vasoprotein Release in Man

Sigma receptors are associated with cortical limbic areas in the primate brain

The Role of Plasma Osmolality, Angiotensin Ii and Dopamine in Vasopressin Release in Man

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