Effect of water and salt intake on pituitary catecholamines in the rat and domestic pig

Holzbauer, Margarethe; Sharman, D. F.; Godden, Urma; Mann, S. P.; Stephens, D.B.

doi:10.1016/0306-4522(80)90041-x

Cited by 39 publications

(14 citation statements)

References 16 publications

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“…Early investigations into the effects of dehydration on tuberohypophyseal DA neurons were limited to measure ments of steady state concentrations of DA in the posterior pituitary; severe dehydration induced by water deprivation and NaCl drinking increased the DA content [2,12,13,22], It was subsequently shown that the rate of DOPA accumu lation (a biochemical index of DA synthesis and neuronal activity, at least in nigrostriatal DA neurons [19]) was selec tively increased in the posterior pituitary at a time when the DA concentrations were unchanged [2,18].…”

Section: Discussionmentioning

confidence: 99%

Changes in the Rate of Dopamine Synthesis in the Posterior Pituitary during Dehydration and Rehydration:Relationship to Plasma Sodium Concentrations

Alper¹,

Demarest²,

Moore³

1982

Neuroendocrinology

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The rate of DOPA accumulation after the administration of a decarboxylase inhibitor (an in vivo estimate of dopamine synthesis) was determined in rat posterior pituitary, median eminence and striatum, regions containing terminals of tuberohypophyseal, tuberoinfundibular and nigrostriatal dopamine neurons, respectively. 3 days of water deprivation increased the hematocrit and the plasma sodium concentration and also increased the rate of DOPA accumulation in the posterior pituitary, but not in the striatum or median eminence. Water deprivation or substitution of 2% NaCl for drinking water for 5 days increased DOPA accumulation in the posterior pituitary and the plasma sodium concentration, while the hematocrit was increased only in the water-deprived group. Following 3 days of water deprivation, access to water for 3 h caused the elevated DOPA accumulation in the posterior pituitary and the plasma sodium concentration to return to control values while the hematocrit remained slightly elevated. Substitution of 2% NaCl for drinking water for 48 h to rats which had been water-deprived for 3 days restored the hematocrit to control, but did not alter the water deprivation-induced increase in plasma sodium concentration or the rate of DOPA accumulation in the posterior pituitary. These results suggest that tuberohypophyseal dopaminergic neurons are regulated, at least in part, by sodium or osmoreceptors.

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Section: Discussionmentioning

confidence: 99%

Changes in the Rate of Dopamine Synthesis in the Posterior Pituitary during Dehydration and Rehydration:Relationship to Plasma Sodium Concentrations

Alper¹,

Demarest²,

Moore³

1982

Neuroendocrinology

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“…The evidence for an involvement of a dopaminergic pathway in the control of ADH release is controversial: exogenous dopamine application into the hypothalamus or into the third ventricle leads to enhanced, unchanged or reduced ADH release (Bridges et al, 1976;Holzbauer et al, 1980;Lightman et al, 1982Racke et al, 1986. Few data are available on an interaction at the site of action of ADH.…”

Section: Introductionmentioning

confidence: 99%

“…Although controversial, there is some evidence for an inhibitory effect of dopamine on ADH secretion from the neurohypophysis (Lightman et al, 1982). Variable effects of exogenously administered dopamine on ADH release have been reported (Forsling et al, 1979;Holzbauer et al, 1980;Racke et al, 1986). Similarly, conflicting results on dopamine content in hypothalamus and hypophysis after water deprivation or salt loading in rats have been reported (Holzbauer et al, 1978).…”

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confidence: 99%

Effect of dopamine antagonists on the urine flow of rats infused with hypotonic saline

Angchanpen

Marin-Grez

Schnermann

1988

British J Pharmacology

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1 The probable involvement of dopamine in the regulation of water excretion was investigated by administering dopamine antagonists intravenously to barbiturate -anaesthetized rats undergoing a water diuresis induced by the infusion of 0.83% glucose with 0.3% NaCl at the rate of 9 ml h-'. 2 Administration of 100l ig of the D,-/D2-dopamine antagonist, haloperidol, reduced the enhanced urine flow of rats infused with the hypotonic solution by 69% (from 75.4 ± 13.0 to 23.6 ± 6.0 pI min-', P<0.01). Similarly, the D,-receptor antagonist, SCH23390, reduced urine flow by 58% (from 77.5 ± 9.2 to 32.7 ± 7.2p fmin-', P <0.01) and the D2-receptor antagonist, sulpiride, by 47% (from 66.2 ± 8.6 to 35.1 ± 6.8 pidmin-', P < 0.05).3 The injection of SCH 23390 increased the urine osmolality from 189.6 ± 27.5 to 479.8 ± 45.8 mosm kg-' (P < 0.05). There was no significant change in sodium and potassium excretion in any of the experiments. Blood pressure (BP) decreased after haloperidol and SCH 23390 injection from control values of 121.7 ± 1.7 and 116.5 ± 7.4 to 113.3 ± 3.3 and 106.0 ± 8.8 mmHg respectively (P < 0.05). 4 To study whether the influence of dopamine antagonists on urine flow during water diuresis depends on antidiuretic hormone (ADH), we administered 0.6 Ag d(CH2)5-D-Phe-Ile-AVP (an ADH antagonist) shortly after the injection of l00 g SCH 23390. The preferential V2 ADH-antagonist abolished the antidiuretic effect of SCH 23390 but did not affect its blood pressure reducing effect (from 118.6 ± 5.6 to 103.2 ± 4.6 mmHg, P <0.01). 5 These results suggest that dopamine antagonists blunted the hypotonic saline-induced diuresis by favouring ADH release through an interference with an inhibitory dopaminergic pathway.

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“…Thus, dopaminergic and noradrenergic nerve fibres innervate this gland (1)(2)(3)(4). There is considerable evidence that dopamine and noradrenaline may play a significant role as local modulators of the release of vasopressin and oxytocin (4)(5)(6)(7)(8)(9).…”

mentioning

confidence: 99%

Effects of Different Opioid Receptor Antagonists on the Electrically‐Evoked Release of Endogenous Dopamine from the Isolated Neural Lobe of the Rat Pituitary Gland in vitro

Racké

Hering

Weber

1990

J Neuroendocrinology

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Isolated neural lobes of the rat pituitary gland were incubated in Krebs-HEPES solution which contained the dopamine uptake inhibitor GBR 12921 and in some experiments additionally pargyline. The release of endogenous dopamine evoked by electrical stimulation of the pituitary stalk was determined by high-performance liquid chromatography with electrochemical detection. (*)-Naloxone increased the evoked dopamine release maximally by 440% (EC,, 209 nM). The (+)-enantiomer of naloxone (up to 10 pM) did not affect the release of dopamine. The preferential rc-opioid receptor antagonist M R 2266 increased the evoked dopamine release maximally by 135% (EC,, 7 nM). M R 2267, the inactive (+)-enantiomer of M R 2266, had no effect on dopamine release. The 8-opioid receptor selective antagonist ICI 174864 increased the release of dopamine maximally by 120% (EC,, 10 nM). The nonselective opioid receptor agonist etorphine up to 10 pM had no effect on the evoked dopamine release. In conclusion, endogenous opioids in the neurohypophysis strongly inhibit the release of endogenous dopamine from this gland. Activation of K-and 8-opioid receptors appears to be involved in the inhibitory action of the endogenous opioids on the neurohypophysial release of dopamine.The rat neurohypophysis contains, beside the classical neurohormones vasopressin and oxytocin, a number of other biologically active neuropeptides and neurotransmitters. Thus, dopaminergic and noradrenergic nerve fibres innervate this gland (1-4). There is considerable evidence that dopamine and noradrenaline may play a significant role as local modulators of the release of vasopressin and oxytocin (4-9). In addition, different opioid peptides are present in the neurohypophysis in high concentrations. They appear to be co-localized with the neurohormones in the neurosecretory nerve endings, those derived from pro-dynorphin with vasopressin and those derived from pro-enkephalin with oxytocin (10-13). In addition, depolarizing stimuli which are known to induce the release of vasopressin and oxytocin (14-16) also evoke the release of the opioid peptides Since the opioid receptor antagonist naloxone increased the release of vasopressin (20, 21) and particularly that of oxytocin (21-28), it was concluded that the endogenous opioids in the neurohypophysis may modulate directly the release of these neurohormones. Furthermore, these opioids also appear to inhibit the release of noradrenaline and dopamine in this gland, since naloxone also enhanced the electrically-evoked release of [3H]-noradrenaline (2 I ) and that of endogenous dopamine (29) from the isolated neurohypophysis. Thus, the endogenous opioids in (1 7-19).the neurohypophysis appear to control the release of several neurotransmitters and neurohormones.It is now clear that opioid receptors consist of several subtypes (30). Therefore, it appears possible that the different opioid peptides in the neurohypophysis may modulate the release of the neurohormones and that of the catecholamines via different opioid recep...

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Effect of water and salt intake on pituitary catecholamines in the rat and domestic pig

Cited by 39 publications

References 16 publications

Changes in the Rate of Dopamine Synthesis in the Posterior Pituitary during Dehydration and Rehydration:Relationship to Plasma Sodium Concentrations

Changes in the Rate of Dopamine Synthesis in the Posterior Pituitary during Dehydration and Rehydration:Relationship to Plasma Sodium Concentrations

Effect of dopamine antagonists on the urine flow of rats infused with hypotonic saline

Effects of Different Opioid Receptor Antagonists on the Electrically‐Evoked Release of Endogenous Dopamine from the Isolated Neural Lobe of the Rat Pituitary Gland in vitro

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