Barrel rotation evoked by intracerebroventricular vasopressin injections in conscious rats. I. Description and general pharmacology

Wurpel, John N.D.; Dundore, Ronald L.; Barbella, Yarisma; Balaban, Carey D.; Keil, L. C.; Severs, Walter B.

doi:10.1016/0006-8993(86)90718-3

Cited by 37 publications

(16 citation statements)

References 21 publications

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“…induced in some rats (15%) a motor disturbance called "barrel rotation." 19 Thus, for the hemodynamic study, we used a smaller dose of AVP (10 ng) that did not evoke this motor abnormality because the phenomenon could have hidden effects on the regional blood flow, particularly in that of the hindquarter. Intravenous AVP increased MAP and regional resistance, especially in the mesenteric and renal beds.…”

Section: Summary Of Cardiovascular Responses (Heart Rate [Hr] and Mmentioning

confidence: 99%

Central vasopressin raises arterial pressure by sympathetic activation and vasopressin release.

1989

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Although central administration of arginine vasopressin (AVP) has been reported to increase arterial pressure mediated by activation of the sympathetic system, we found that peripheral blockade of sympathetic transmission did not attenuate this pressor response. To elucidate the mechanism, rats were pretreated with either phentolamine (3 mg/kg), chlorisondamine (2.5 mg/kg), a vasopressin V! receptor antagonist d(CH 2 )sTyr(Me)AVP (AVP-X) (10 /xg/kg), or the combinations of phentolamine and AVP-X or chlorisondamine and AVP-X. The pressor response to intracerebroventricular injection of AVP in unrestrained conscious rats was reduced but not significantly altered by intravenous injection of phentolamine or AVP-X; however, combined treatment with these agents abolished the response. To determine that the amount of central AVP leaked to the periphery did not contribute to the pressor effect, tritiated AVP and AVP (100 ng total) were injected intracerebroventricularly. Blood samples collected at 0, 3, and 30 minutes after injection showed that radioactivity in plasma was primarily metabolites and that the amount of intact AVP estimated to leak from the brain was too low to produce a pressor effect. 1 Despite the number of papers related to central actions of AVP, the mechanism of the pressor action induced by this centrally injected peptide remains unclear.AVP-containing neurons project from the paraventricular and supraoptic nuclei to brainstem regions such as the nucleus tractus solitarius (NTS). Also, in several regions of the brain specific binding sites for AVP that play a role in central regulation of arterial pressure have been reported.2 MicroinjecFrom the Department of Pharmacology and the Cardiovascular Center, the University of Iowa College of Medicine, Iowa City, Iowa.Supported by Grant HLB-14388 from the National Institutes of Health and by Roussel-Uclaf, Paris, France.This manuscript from the University of Iowa was sent to Carlos M. Ferrario, Guest Editor, for review by expert referees, for editorial decision, and for final disposition.Address for reprints: Michael J. Brody, PhD, University of Iowa, Department of Pharmacology, 2-210 Bowen Science Building, Iowa City, IA 52242. tions of AVP in the NTS raise arterial pressure 34 and increase turnover of catecholamine in this nucleus.5 AVP is stored in the neural lobe of the pituitary gland and can be released into the bloodstream by several central 6 -9 and peripheral 10 stimuli. It has also been indicated that this peptide is present in the cerebrospinal fluid. 11It has been reported that the increase in arterial pressure produced by central injection of AVP is mediated by increased sympathetic outflow.1213 If this were the only mechanism, then blockade of sympathetic transmission should prevent this pressor effect. However, in recent studies, we found that neither ganglionic nor a-adrenergic blockade significantly altered the pressor response. Therefore, the purpose of the present study was to characterize the mechanism of the pressor action evoked by...

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Section: Summary Of Cardiovascular Responses (Heart Rate [Hr] and Mmentioning

confidence: 99%

Central vasopressin raises arterial pressure by sympathetic activation and vasopressin release.

1989

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“…Barrel rotation (BR) is an intense motor disturbance which follows the administra tion of arginine vasopressin (AVP) into the central nervous system (CNS) [1,2], The syndrome induced by intracerebroventricu lar (IVT) AVP includes ataxia, swaying, prostration with spastic limb abduction, and rotations along the long axis of the body (BR). Earlier reports suggest that AVP-induced BR has a significant cerebellar and/or vestibular component [1,2], Injection of AVP by the IVT route usually causes nystag mus prior to BR, and some experimental paradigms that decrease vestibular and/or visual input to the CNS block the motor component.…”

Section: Introductionmentioning

confidence: 99%

“…Earlier reports suggest that AVP-induced BR has a significant cerebellar and/or vestibular component [1,2], Injection of AVP by the IVT route usually causes nystag mus prior to BR, and some experimental paradigms that decrease vestibular and/or visual input to the CNS block the motor component. Rats are 'sensitized' by pre-ex posure to IVT-AVP.…”

Section: Introductionmentioning

confidence: 99%

“…That is, a greater pro portion of rats display the behavior after 0.5 pg IVT-AVP when preceded by 1 pg given 48 h earlier, and all rats responding to the first dose respond to the second injection. This 'sensitization' can also be inhibited by some paradigms which disrupt visual/vestibular integration [1,2], Receptors for AVP have been localized in areas of the CNS that are unrelated to the hypothalamo-pituitary axis [3,4], Localiza tion of receptors in other brain areas, includ ing cerebellum, cortex, brainstem, and hip pocampus, suggests that AVP exerts physio logical effects at these sites. Exogenous AVP exerts multiple effects on the CNS [1].…”

Section: Introductionmentioning

confidence: 99%

“…This 'sensitization' can also be inhibited by some paradigms which disrupt visual/vestibular integration [1,2], Receptors for AVP have been localized in areas of the CNS that are unrelated to the hypothalamo-pituitary axis [3,4], Localiza tion of receptors in other brain areas, includ ing cerebellum, cortex, brainstem, and hip pocampus, suggests that AVP exerts physio logical effects at these sites. Exogenous AVP exerts multiple effects on the CNS [1]. We have measured regional cerebral metabolic rates for glucose (rCMRglu) during AVPinduced BR to assist in identifying motor structures responsive to the peptide.…”

Section: Introductionmentioning

confidence: 99%

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Regional Cerebral Glucose Utilization during Vasopressin-Induced Barrel Rotations or Bicuculline-Induced Seizures in Rats

Wurpel¹,

Dundore²,

Bryan³

et al. 1988

Pharmacology

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Regional cerebral metabolic rates of glucose (rCMRglu) were measured in conscious rats grouped according to three treatments: control, bicuculline (5.5 mg/kg s.c), and intracerebroventricular arginine vasopressin (0.5 μg/5 μl). Rats in the latter group were pre-exposed to the peptide 48 h earlier to render them 100% susceptible to a motor output termed barrel rotation (BR). Marked increases in rCMRglu occurred in all brain areas investigated after bicuculline. Increases after intracerebroventricular arginine vasopressin were smaller and occurred in fewer brain areas. Opposite to bicuculline, arginine vasopressin reduced rCMRglu in hippocampus and auditory cortex. The data confirm marked stimulation of rCMRglu during bicuculline-induced seizures and provide initial data for an endogenous peptide that causes BR. Generalized seizures and BR may share some neural substrates, but they produce distinct changes in rCMRglu. The rCMRglu changes are compatible with the interpretation that BR is initiated by brainstem/cerebellar areas that process visual-vestibular information, with subsequent involvement of higher brain structures.

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NMDA receptor and NO mediate ET-1-induced behavioral and cardiovascular effects in periaqueductal gray matter of rats

et al. 2001

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Endothelin-1 (ET-1), a novel and potent vasoconstrictor in blood vessel, is known to have some functions in the rat central nervous system (CNS). In order to investigate the central functions of ET-1, ET-1 was administered to the periaqueductal gray area (PAG) of anesthetized rats to induce barrel rolling and increase the arterial blood pressure (ABP). ET-1 had a modulatory effect on central cardiovascular and behavioral control. The selective N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 (3 micromol/kg, i.p.) blocked the ET-1 induced responses, and both the nitric oxide synthase (NOS) inhibitor L-NAME (N-nitro-L-arginine methylester 1 mmol/rat) and the nitric oxide (NO) scavenger hemoglobin (15 nmol/rat) had similar effects in reducing the ET-1 (10 pmol/rat)-induced behavioral changes and ABP elevation. However, NO donor sodium nitroprusside (SNP 10 microg, 1 microg/rat) decreased the ET-1 induced ABP elevation, and recovered the ET-1-induced barrel rolling effect that was reduced by MK-801. These results suggest that ET-1 might have neuromodulatory functions such as ABP elevation and barrel rolling induction in the PAG of the rats via the NMDA receptor and NO.

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Barrel rotation evoked by intracerebroventricular vasopressin injections in conscious rats. I. Description and general pharmacology

Cited by 37 publications

References 21 publications

Central vasopressin raises arterial pressure by sympathetic activation and vasopressin release.

Central vasopressin raises arterial pressure by sympathetic activation and vasopressin release.

Regional Cerebral Glucose Utilization during Vasopressin-Induced Barrel Rotations or Bicuculline-Induced Seizures in Rats

NMDA receptor and NO mediate ET-1-induced behavioral and cardiovascular effects in periaqueductal gray matter of rats

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