Central infusion of vasopressin decreased plasma vasopressin concentration in dogs

Wang, B. C.; Share, Leonard; Crofton, J. T.

doi:10.1152/ajpendo.1982.243.5.e365

Cited by 16 publications

(9 citation statements)

References 19 publications

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“…Functional evidence suggests that the effects of vasopressin on electrical activity are likely to be inhibitory. Intracerebroventricular injection of vaso-Vasopressin effects on supraoptic nucleus neurons 2533 pressin decreases plasma vasopressin concentration (Wang et al, 1982), while V I N Z antagonists enhance vasopressin release into the blood in response to osmotic stimulation (Liu et al, 1996), but the site of action of vasopressin cannot be inferred from these experiments.…”

Section: Introductionmentioning

confidence: 97%

Autoinhibition of Supraoptic Nucleus Vasopressin Neurons In Vivo: A Combined Retrodialysis/Electrophysiological Study in Rats

Ludwig

Leng

1997

Eur J of Neuroscience

129

119

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To examine the role of endogenous vasopressin on the electrical activity of vasopressin neurons within the supraoptic nucleus of the rat brain in vivo, we have developed a novel technical approach for administering neuroactive drugs directly into the extracellular environment of the neuronal dendrites. A microdialysis probe was used for controlled local drug administration into the dendritic area of the nucleus during extracellular recording of single neurons in vivo. Vasopressin or selective V1 receptor antagonists were administered for between 10 and 30 min via a U-shaped microdialysis probe placed flat on the surface of the supraoptic nucleus after transpharyngeal exposure of the nucleus in urethane-anaesthetized rats. Microdialysis administration (retrodialysis) of vasopressin inhibited vasopressin neurons by reducing their firing rate, sometimes to total inactivity. Retrodialysis of V1-receptor antagonists partially reversed the effect of vasopressin, and a subsequent vasopressin administration was not effective in reducing the activity of these neurons, suggesting a receptor-mediated action of endogenous vasopressin. In addition, the duration of the periods of activity and the mean frequency during the active phase were increased in vasopressin neurons after retrodialysis of V1-receptor antagonist, indicating a physiological role of endogenous vasopressin. Neither vasopressin nor the antagonists altered the activity of continuously firing oxytocin neurons. Thus, vasopressin released within the supraoptic nucleus may act via V1 receptors located specifically on vasopressin neurons to regulate their phasic activity by an auto-inhibitory action. Since vasopressin release from the dendrites of vasopressin neurons is increased and prolonged after various forms of stimulation, it is proposed that this mechanism will act to limit excitation of vasopressin neurons, and hence secretion from the neurohypophysis. In addition, combined in vivo retrodialysis/ single cell recording allows controlled introduction of neuroactive substances into the extracellular fluid in the immediate vicinity of recorded neurons. This is shown to provide a novel approach to study neurotransmitter actions on supraoptic neurons in vivo.

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Section: Introductionmentioning

confidence: 97%

Autoinhibition of Supraoptic Nucleus Vasopressin Neurons In Vivo: A Combined Retrodialysis/Electrophysiological Study in Rats

Ludwig

Leng

1997

Eur J of Neuroscience

129

119

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“…It has been reported that vasopressin administered cen trally causes a decrease in the plasma concentration o f va sopressin [14]. This indicates that vasopressin occurring within the central nervous system may be able to alter its own release into the circulation.…”

Section: Discussionmentioning

confidence: 99%

“…It seems likely, therefore, that under the conditions o f the present experiment there is probably no negative feedback inhibition by vasopressin on its own release. Thus, the reduction in plasma vasopressin concentration induced by the central administration of this hormone [14] is caused by an action of vasopressin at sites remote from areas that would be affected by circulating hormone. Fur thermore, it is likely that the only way that circulating vaso pressin can alter its own release is in a long negative feed back loop involving its actions on blood pressure, blood vo lume, and plasma osmolality.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, peripherally circulating va sopressin seems to manifest some of its cardiovascular ac tions via the central nervous system. Vasopressin adminis tered centrally has previously been shown to effect blood pressure [13] and reduce the plasma vasopressin concentra tion [14]. It is, however, of interest to establish whether pe ripherally-released vasopressin can act via the central ner vous system to alter its own release.…”

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confidence: 99%

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Effect of Vertebral, Carotid and Intravenous Infusions of Lysine Vasopressin on Plasma Vasopressin and Cardiovascular Function

Brooks¹,

Share²,

Crofton³

et al. 1984

Neuroendocrinology

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The cardiovascular and vasopressin-releasing effects of vertebral artery, carotid artery and intravenous (i.v.) infusions of lysine vasopressin (150 µU/kg·min) were studied in anesthetized dogs. Vertebral and carotid artery infusions of lysine vasopressin led to similar decreases in cardiac output as i.v. infusions. Heart rate, however, decreased to a greater extent with vertebral and carotid artery infusions of lysine vasopressin than i.v. infusions. There were no changes in either mean arterial blood pressure or the plasma vasopressin concentration. The results indicate that peripheral vasopressin: (1 has a central effect to reduce heart rate; (2) has a peripheral effect on the heart to reduce cardiac output, and (3) probably does not feed back to inhibit its own release.

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“…In several studies, therefore, the effect of central administration of AVP on body water metabolism has been examined. A central dipsogenic effect of centrally applied AVP has been reported (Szczepanska-Sadowska, Sobocinska & Sadowski, 1982) and release of pituitary AVP was shown to be inhibited following intracerebroventricular injection or infusion of AVP (Bhargava, Kulshrestha & Srivastava, 1977;Wang, Share & Crofton, 1982). However, in other studies no effects of such AVP treatments have been found on peripheral hydration and consummatory behaviour (Severs, Keil & Klase, 1978;Jerome, Barbella, Wurpel et al 1983).…”

mentioning

confidence: 99%

Osmoregulation in rats with long-term enhanced cerebrospinal fluid levels of vasopressin or vasoactive intestinal polypeptide

Kruisbrink¹,

Heerikhuize²,

Boer³

1988

Journal of Endocrinology

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The cerebrospinal fluid level of arginine vasopressin (AVP) or vasoactive intestinal polypeptide (VIP) was enhanced chronically by implantation of a device for controlled drug delivery in the lateral ventricle of the rat. Urine production, water consumption, urine osmolality as well as urinary AVP excretion were then measured for a period of 26 days. During this period the rats were studied under normal hydration and under conditions of osmotic stress induced by water deprivation (2 days) and the drinking of 2% (w/v) NaCl (6 days), in order to see whether the capacity of central systems to react adequately to osmotic stimuli was affected by high central peptide levels. Immediately after the central AVP treatment was started, a temporary increase was found in urinary AVP levels which was not accompanied by a change in any of the other parameters but which decreased again to control levels within 10 days. After this burst of AVP excretion, AVP-treated rats showed a tendency during periods of normal hydration for a lower urine osmolality, combined with a higher water intake and urine production without changes in urinary AVP excretion. Since there was no clear-cut correlation between urinary AVP excretion and body water turnover, this could still indicate a slowly acquired and slight inhibition of pituitary AVP release by long-term centrally administered AVP. However, the capacity of these rats to respond to osmotic stimuli was not different from the controls. In the VIP-treated rats a slight but significant reduction in urine production was found in all three periods of normal hydration.(ABSTRACT TRUNCATED AT 250 WORDS)

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Central infusion of vasopressin decreased plasma vasopressin concentration in dogs

Cited by 16 publications

References 19 publications

Autoinhibition of Supraoptic Nucleus Vasopressin Neurons In Vivo: A Combined Retrodialysis/Electrophysiological Study in Rats

Autoinhibition of Supraoptic Nucleus Vasopressin Neurons In Vivo: A Combined Retrodialysis/Electrophysiological Study in Rats

Effect of Vertebral, Carotid and Intravenous Infusions of Lysine Vasopressin on Plasma Vasopressin and Cardiovascular Function

Osmoregulation in rats with long-term enhanced cerebrospinal fluid levels of vasopressin or vasoactive intestinal polypeptide

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