Regional distribution of putative vasopressin receptors in rat brain and pituitary by quantitative autoradiography.

Brinton, Roberta Dı́az; Gee, Kelvin W.; Wamsley, James K.; Davis, Thomas P.; Yamamura, Henry I.

doi:10.1073/pnas.81.22.7248

Cited by 97 publications

(60 citation statements)

References 31 publications

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“…This effect, if present, seems to be restricted to penumbral tissue, because inhibition of AVP V 1 receptors does not affect CBF in the infarct core (Figure 1). Another explanation for AVP V 1 receptor-mediated neuroprotection might be that AVP V 1 receptors are widely expressed in the brain parenchyma (Brinton et al, 1984;Pearlmutter et al, 1988;Phillips et al, 1988;Young et al, 1999;Tribollet et al, 1999;Fernandez et al, 2001) where they have been implicated in intracellular calcium mobilization, activation of NMDA receptors, and superoxide anion generation (Urban and Killian, 1990;Hess et al, 1991;Gouzenes et al, 1999;Armstead, 2001), all conditions well known to be associated with neuronal cell death after cerebral ischemia (Lo et al, 2003). Accordingly, the positive effect AVP V 1 receptor inhibition on cell death might also be explained by a reduction of glutamate-and superoxide anion-mediated toxicity, as also discussed previously (Tanaka et al, 1994).…”

Section: Alternative Mechanisms Of Avp-mediated Brain Damagementioning

confidence: 99%

Role of Arginine Vasopressin V₁ and V₂ Receptors for Brain Damage After Transient Focal Cerebral Ischemia

Vakili

Kataoka

Plesnila

2005

J Cereb Blood Flow Metab

130

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Brain edema formation is one of the most important mechanisms responsible for brain damage after ischemic stroke. Despite considerable efforts, no specific therapy is available yet. Arginine vasopressin (AVP) regulates cerebral water homeostasis and has been involved in brain edema formation. In the current study, we investigated the role of AVP V 1 and V 2 receptors on brain damage, brain edema formation, and functional outcome after transient focal cerebral ischemia, a condition comparable with that of stroke patients undergoing thrombolysis. C57/BL6 mice were subjected to 60-min middle cerebral artery occlusion (MCAO) followed by 23 h of reperfusion. Five minutes after MCAO, 100 or 500 ng of [deamino-Pen(1), O-Me-Tyr(2), Arg (8) .2% in controls; Po0.001), blood-brain barrier disruption by 75% (Po0.001), and functional deficits 24 h after ischemia, while V 2 receptor inhibition had no effect. The current findings indicate that AVP V 1 but not V 2 receptors are involved in the pathophysiology of secondary brain damage after focal cerebral ischemia. Although further studies are needed to clarify the mechanisms of neuroprotection, AVP V 1 receptors seem to be promising targets for the treatment of ischemic stroke.

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Section: Alternative Mechanisms Of Avp-mediated Brain Damagementioning

confidence: 99%

Role of Arginine Vasopressin V₁ and V₂ Receptors for Brain Damage After Transient Focal Cerebral Ischemia

Vakili

Kataoka

Plesnila

2005

J Cereb Blood Flow Metab

130

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“…Nevertheless, in these regions, the presence of OT and VP receptors is subject to controversy. Indeed, using autoradiography, many authors have detected [3H]OT or ['HIVP labelling in the neural lobe (10,(18)(19)(20)(21)(22), but few of them have stated that this labelling was not displaced or only partly so by an excess of unlabelled hormone ( 1 I , 13). The complete disappearance of [3H]VP binding after stalk transection indicated that the binding sites were presynaptic (21).…”

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confidence: 99%

“…The absence, or very low levels, of [3H]VP or [3H]OT binding has been reported by some authors (21)(22)(23) in Brattleboro rats, while observations reported by Brinton et 01. (18) (20).…”

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confidence: 99%

Neurophysins, rather than Receptors, are Involved in [³H]Oxytocin and [³H]Vasopressin Binding Detected by Autoradiography in the Hypothalamo‐Neurohypophyseal System

Freund-Mercier

Stoeckel

Waeber

et al. 1991

J Neuroendocrinology

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The goal of the present experiments was to analyse the binding of oxytocin (OT) and vasopressin (VP) Specific neurohypophyseal hormone-binding sites have been characterized and localized in the brain using binding techniques to acellular preparations (for examples see 1-6) and/or autoradiography (for examples see 7-14). Two types of binding sites have thus been clearly defined, oxytocin (0T)-binding sites, which havc nanomolar-range affinity for O T and vasopressin (VP), and VP-binding sites, which have nanomolar-range affinity for VP and a much lower affinity for OT (3, 11). In the rat brain, the two types of sites have quite distinct distributions: OT-binding sites occur mainly in the ventral subiculum, several nuclei of the amygdala, the ventromedial hypothalamic nucleus, the bed nucleus of the stria terminalis and the olfactory tubercle (8-11, 13, 14); VP-binding sites are mainly detected in the nucleus of the solitary tract, several thalamic nuclei, the suprachiasmatic nucleus, the fundus striati and the lateral septa1 nucleus (7, 8, 10-13). The pharmacological characteristics (high affinity, low capacity, saturability) of the OT and VP sites detected in such locations (l-6), and their occurrence in areas where exogenous O T or VP can affect the electrical response of neurons (1 5-17), suggest that they are functional receptors.Binding of neurohypophyseal hormones has also been shown to occur in the hypothalamo-neurohypophyseal system, i.e. the supraoptic nuclei (SON), the paraventricular nuclei (PVN) and It is questionable whether receptors are involved in OT and VP binding in the hypothalamo-neurohypophyseal system. OT and VP may bind to neurophysins which are associated with these peptides in the secretory vesicles, scattered in the perikarya and the axons, and highly concentrated in the nerve endings in

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“…Immuno-electron microscopic studies have shown that the AVP present in paraventricular neurones is contained within vesicle-like structures (Buijs & Swaab, 1979;Voorn & Buijs, 1983). Moreover, binding studies have revealed specific binding sites for AVP on neural membranes in the NTS (Dorsa et al, 1983;Brinton et al, 1984). This 'Author for correspondence.…”

Section: Introductionmentioning

confidence: 99%

Cardiovascular effects of injections of vasopressin into the nucleus tractus solitarius in conscious rats

King

Pang

1987

British J Pharmacology

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1The effects of injections of arginine vasopressin (AVP) into the nucleus tractus solitarius (NTS) on mean arterial pressure (MAP), heart rate (HR) and plasma concentrations of noradrenaline and adrenaline were investigated in conscious, unrestrained rats. 2 Injection of 2 ng AVP into the NTS significantly increased MAP but not plasma catecholamine concentrations, while injection of 10 ng AVP significantly increased MAP and plasma noradrenaline and adrenaline levels. 3 Neither dose of AVP produced any change in HR. The vehicle did not affect MAP, HR or plasma catecholamine levels. 4 Injection of a specific pressor antagonist of AVP, d(CH2)5Tyr-(Me)AVP (10 ng), did not change MAP, HR or plasma noradrenaline or adrenaline levels. 5 These results suggest that the NTS is a central site of the pressor action of AVP. However, since the injection of the AVP antagonist did not reduce MAP or plasma noradrenaline or adrenaline levels, it suggests that AVP does not act tonically at the NTS to influence sympathoadrenal outflow.

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Regional distribution of putative vasopressin receptors in rat brain and pituitary by quantitative autoradiography.

Cited by 97 publications

References 31 publications

Role of Arginine Vasopressin V₁ and V₂ Receptors for Brain Damage After Transient Focal Cerebral Ischemia

Role of Arginine Vasopressin V₁ and V₂ Receptors for Brain Damage After Transient Focal Cerebral Ischemia

Neurophysins, rather than Receptors, are Involved in [³H]Oxytocin and [³H]Vasopressin Binding Detected by Autoradiography in the Hypothalamo‐Neurohypophyseal System

Cardiovascular effects of injections of vasopressin into the nucleus tractus solitarius in conscious rats

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Regional distribution of putative vasopressin receptors in rat brain and pituitary by quantitative autoradiography.

Cited by 97 publications

References 31 publications

Role of Arginine Vasopressin V1 and V2 Receptors for Brain Damage After Transient Focal Cerebral Ischemia

Role of Arginine Vasopressin V1 and V2 Receptors for Brain Damage After Transient Focal Cerebral Ischemia

Neurophysins, rather than Receptors, are Involved in [3H]Oxytocin and [3H]Vasopressin Binding Detected by Autoradiography in the Hypothalamo‐Neurohypophyseal System

Cardiovascular effects of injections of vasopressin into the nucleus tractus solitarius in conscious rats

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Role of Arginine Vasopressin V₁ and V₂ Receptors for Brain Damage After Transient Focal Cerebral Ischemia

Role of Arginine Vasopressin V₁ and V₂ Receptors for Brain Damage After Transient Focal Cerebral Ischemia

Neurophysins, rather than Receptors, are Involved in [³H]Oxytocin and [³H]Vasopressin Binding Detected by Autoradiography in the Hypothalamo‐Neurohypophyseal System