Dynorphin-(1-13) is a potent in vivo suppressor of vasopressin levels in the rat

Haaf, Jeroen Alexander ten; Maigret, C.; Andringa-Bakker, Els A.D.; Greidanus, T.B. van Wimersma

doi:10.1530/acta.0.1140096

Cited by 24 publications

(13 citation statements)

References 14 publications

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“…Hence, it seems that U50488H may inhibit AVP secre tion via the posterior pituitary. Meanwhile, it was reported that dynorphin, an endogenous K-opioid agonist, binds to some opioid receptors in the neurohypophysis [9], and dynorphin, per se, was reported to exert a potent sup pressive action on plasma AVP [10]. These observations also support our hypothesis.…”

Section: Discussionsupporting

confidence: 89%

Effect of the Opioid Kappa-Receptor Agonist U50488H on the Secretion of Arginine Vasopressin

Oiso

Iwasaki²,

Kondo³

et al. 1988

Neuroendocrinology

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The effect of U50488H, a potent opioid K-receptor agonist, was investigated on the urine volume and on the secretion of arginine vasopressin (AVP) in response to dehydration or hyperosmolar or hypovolemic stimulation in conscious rats. This agonist markedly increased the urine volume in normally hydrated rats and suppressed plasma AVP in a dose-dependent manner in rats given hyperosmolar saline. This suppression of plasma AVP was completely reversed by concurrent injection of naloxone. U50488H also inhibited the release of AVP in dehydrated or hypovolemic rats. These findings indicate that the diuresis induced by U50488H is mainly caused by the suppression of plasma AVP. They also suggest that the K-opioid receptor plays an important role in regulating the secretion of AVP.

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Section: Discussionsupporting

confidence: 89%

Effect of the Opioid Kappa-Receptor Agonist U50488H on the Secretion of Arginine Vasopressin

Oiso

Iwasaki²,

Kondo³

et al. 1988

Neuroendocrinology

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“…Some studies demonstrated diureses or a decrease in vasopressin release by K-agonists injected into the ventri cle (14)(15)(16). This is not consistent with our present results.…”

Section: Discussionmentioning

confidence: 99%

“…Met-enkephalin is reported to show di ureses by intracerebroventricular injection and anti diureses by microinjection into nuclei (6,33). 2) In the studies for the diureses or decrease in vasopressin release by the K-agonists, conscious and non-hydrated (14 16), water-deprived (14), hydrated (16) or angiotensin II stimulated (15) rats are used. Basal vasopressin level in the plasma under these conditions will be higher than that under the ethanol-anesthetized, ethanol-infused and hydrated condition in the present study, although under the present condition, it is possible to produce diureses by some drugs (this study, ref.…”

Section: Discussionmentioning

confidence: 99%

“…These antidiuretic effects, at least in part, appear to be induced by increased vasopressin re lease, although there are some reports that the opioid agonists show decrease or have no effect on the firing rate of vasopressin-containing neurons or vasopressin release (4,(9)(10)(11)(12)(13). On the other hand, c-agonists injected into the ventricle decrease vasopressin release and induce diuretic effects (14)(15)(16). Systemic administered K-agonists also elic it the same effects, which are suggested to be mediated through K-receptors on the neurohypophysis (16)(17)(18)(19).…”

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confidence: 99%

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Microinjection of Dynorphin into the Supraoptic and Paraventricular Nuclei Produces Antidiuretic Effects through Vasopressin Release

Tsushima

Mori

Matsuda

1993

Japanese Journal of Pharmacology

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ABSTRACT-The mechanisms for the antidiuretic effects of dynorphin (DYN), an endogenous K-agonist, microinjected into the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei were investigated. DYN decreased the urine outflow rate dose-dependently from 5 to 20 nmol in the SON and PVN, and it in creased vasopressin release. Microinjection of des-Tyr-DYN (a non-opioid peptide) into the SON produced antidiuretic effects with similar potency to that of the DYN-induced effects. However, in the PVN, the effects of des-Tyr-DYN were very markedly weaker than those of DYN. The DYN-induced antidiureses in the SON were partially inhibited by phenoxybenzamine, timolol and atropine, but not by naloxone. Those in the PVN were partially inhibited by naloxone, timolol and atropine, but not by phenoxybenzamine. Syn thetic specific K-agonists, U50,488H and Tyr-Gly-Gly-Phe-Leu-Arg-Arg-Ile-Arg-Pro-Arg-Leu-Arg-Gly 5 aminopentylamide (DAKLI), microinjected into the PVN also produced antidiuretic effects in a dose-de pendent manner. The order of antidiuretic potency was DAKLI > DYN > U50,488H, which was the same as that of K-receptor binding affinity. The DAKLI-induced antidiureses in the PVN were not inhibited by nalox one. These results suggested that DYN caused antidiureses by vasopressin release, through adrenergic and cholinergic mechanisms in the SON and PVN. Only the DYN-induced effects in the PVN were mediated, at least partially, through opioid receptors, perhaps the x-subtype. Immunohistochemical studies show the presence of fibers and terminals of opioid neurons (1-3) in the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei. Also, cell bodies of vasopressin-containing neurons are localized in these nuclei. Numerous reports suggest that opioid neurons in the hypothalamus, the SON or PVN regulate the urine outflow rate. Intra cerebroventricular injection and microinjection into the nuclei of p and o-opioid agonists decrease the urine outflow rate (4 8). These antidiuretic effects, at least in part, appear to be induced by increased vasopressin re lease, although there are some reports that the opioid agonists show decrease or have no effect on the firing rate of vasopressin-containing neurons or vasopressin release (4, 9-13). On the other hand, c-agonists injected into the ventricle decrease vasopressin release and induce diuretic effects (14-16). Systemic administered K-agonists also elic it the same effects, which are suggested to be mediated through K-receptors on the neurohypophysis (16-19).In our preliminary study, however, microinjection of dynorphin(1-13) (DYN), an endogenous K-agonist (20, 21) which co-exists with vasopressin (22), into the SON and PVN decreased the urine outflow rate (23). Thus, we investigated the mechanisms of the DYN-induced anti diuretic effects in this study. MATERIALS AND METHODSMale Wistar rats (280-330 g), starved overnight but allowed free access to water, were used. They were orally loaded with tap water (5 ml/100 g body weight); and 45 min later, they were anesthetize...

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“…On the other hand, i.c.v. injection of dynorphin or bremazocine, K-agonists, produces the oppo site effects (16,17). Also, we have reported the antidiuret ic effect induced by microinjection of morphine or fen tanyl into the nuclei (18,19).…”

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confidence: 93%

Effects of D-Ala2-D-Leu5-Enkephalin, Microinjected into the Supraoptic and Paraventricular Nuclei, on Urine Outflow Rate

Tsushima

Mori

Matsuda

1993

Japanese Journal of Pharmacology

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ABSTRACT-The effects of D-Ala2-D-Leu5-enkephalin (DADL, a o-opioid agonist), microinjected directly into the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei, on urine outflow rate, urinary osmotic pressure, blood pressure, heart rate, respiratory rate and rectal temperature were investigated in water-loaded and ethanol-anesthetized rats. The microinjection of DADL into both the nuclei decreased urine outflow rate in a dose-dependent manner with an increase in urinary osmotic pressure, but did not change the other recorded parameters. The DADL-induced antidiuretic effect in the SON was inhibited by naloxone, but not by atropine, phenoxybenzamine, timolol nor a vasopressin antagonist, d(CH2)5-D Tyr(Et)VAVP. The effect in the PVN was inhibited by naloxone, atropine, timolol and d(CH2)5-D Tyr(Et)VAVP, but not by phenoxybenzamine. These results suggest that DADL causes antidiuretic effects mediated through opioid receptors in both the SON and PVN, and the underlying mechanisms are different between them. Involvement of o-opioid receptors in the DADL-induced antidiureses was discussed.

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Dynorphin-(1-13) is a potent in vivo suppressor of vasopressin levels in the rat

Cited by 24 publications

References 14 publications

Effect of the Opioid Kappa-Receptor Agonist U50488H on the Secretion of Arginine Vasopressin

Effect of the Opioid Kappa-Receptor Agonist U50488H on the Secretion of Arginine Vasopressin

Microinjection of Dynorphin into the Supraoptic and Paraventricular Nuclei Produces Antidiuretic Effects through Vasopressin Release

Effects of D-Ala2-D-Leu5-Enkephalin, Microinjected into the Supraoptic and Paraventricular Nuclei, on Urine Outflow Rate

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