Central effects of morphine, levorphanol, (-)-methadone and the opioid-like peptides β-endorphin and D-alanine2-methionine enkephalinamide on urine volume outflow and electrolytes

J. P. Huidobro-Toro, F. Huidobro

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

The intraventricular injection of 10 to 30 nmol of morphine, (-)-methadone or levorphanol caused a reduction in the volume of the urine output in rats previously hydrated with 0.5% sodium chloride. The decrease in urine outflow was associated with a dose-dependent reduction in the concentration of urine Na+ and K+. Two opioid-like peptides: β-endorphin and D-alanine2 methionine enkephalinamide shared this morphine action. On a molar basis, β-endorphin was about 100 times more potent than morphine to cause an equivalent antidiuresis. Naloxone injected i.p. antagonized the response of centrally administered morphine or β-endorphin on urine formation and composition. In addition, (+)-methadone or dextrorphan injected into the cerebral ventricles were considerably less active than their corresponding stereoisomers. N-methyl morphine injected i.p. was completely inactive up to doses that caused signs of toxicity; however, when injected into the lateral cerebral ventricles, it produced a decrease in the urine outflow and a reduction in the concentration of urine electrolytes. The pattern of changes in urine electrolytes produced by morphine and surrogates as well as the opioid-like peptides was in marked contrast to that caused by the i.p. administration of vasopressin. Whereas the i.p. administration of antidiuretic hormone caused oliguria and a large increase in the urine concentration of Na+ and K+, all the opiates produced at comparable antidiuresis a marked reduction in urine electrolytes. Results suggest that the opiates and the opioid-like peptides selectively activate central opiate receptors to produce changes in urine formation and composition. Results are discussed in relation to probable central opiate mechanisms controlling the production and formation of urine.

Original languageEnglish
Pages (from-to)579-585
Number of pages7
JournalJournal of Pharmacology and Experimental Therapeutics
Volume217
Issue number3
Publication statusPublished - 1981
Externally publishedYes

Fingerprint

Levorphanol
Endorphins
Opioid Peptides
Methadone
Morphine
Electrolytes
Urine
Opiate Alkaloids
Cerebral Ventricles
Vasopressins
Met-enkephalinamide
Dextrorphan
Intraventricular Injections
Oliguria
Stereoisomerism
Lateral Ventricles
Opioid Receptors
Naloxone
Sodium Chloride

ASJC Scopus subject areas

  • Pharmacology

Cite this

@article{44e130223c584fd3a58c7b78f0cfcff5,
title = "Central effects of morphine, levorphanol, (-)-methadone and the opioid-like peptides β-endorphin and D-alanine2-methionine enkephalinamide on urine volume outflow and electrolytes",
abstract = "The intraventricular injection of 10 to 30 nmol of morphine, (-)-methadone or levorphanol caused a reduction in the volume of the urine output in rats previously hydrated with 0.5{\%} sodium chloride. The decrease in urine outflow was associated with a dose-dependent reduction in the concentration of urine Na+ and K+. Two opioid-like peptides: β-endorphin and D-alanine2 methionine enkephalinamide shared this morphine action. On a molar basis, β-endorphin was about 100 times more potent than morphine to cause an equivalent antidiuresis. Naloxone injected i.p. antagonized the response of centrally administered morphine or β-endorphin on urine formation and composition. In addition, (+)-methadone or dextrorphan injected into the cerebral ventricles were considerably less active than their corresponding stereoisomers. N-methyl morphine injected i.p. was completely inactive up to doses that caused signs of toxicity; however, when injected into the lateral cerebral ventricles, it produced a decrease in the urine outflow and a reduction in the concentration of urine electrolytes. The pattern of changes in urine electrolytes produced by morphine and surrogates as well as the opioid-like peptides was in marked contrast to that caused by the i.p. administration of vasopressin. Whereas the i.p. administration of antidiuretic hormone caused oliguria and a large increase in the urine concentration of Na+ and K+, all the opiates produced at comparable antidiuresis a marked reduction in urine electrolytes. Results suggest that the opiates and the opioid-like peptides selectively activate central opiate receptors to produce changes in urine formation and composition. Results are discussed in relation to probable central opiate mechanisms controlling the production and formation of urine.",
author = "Huidobro-Toro, {J. P.} and F. Huidobro",
year = "1981",
language = "English",
volume = "217",
pages = "579--585",
journal = "Journal of Pharmacology and Experimental Therapeutics",
issn = "0022-3565",
publisher = "American Society for Pharmacology and Experimental Therapeutics",
number = "3",

}

TY - JOUR

T1 - Central effects of morphine, levorphanol, (-)-methadone and the opioid-like peptides β-endorphin and D-alanine2-methionine enkephalinamide on urine volume outflow and electrolytes

AU - Huidobro-Toro, J. P.

AU - Huidobro, F.

PY - 1981

Y1 - 1981

N2 - The intraventricular injection of 10 to 30 nmol of morphine, (-)-methadone or levorphanol caused a reduction in the volume of the urine output in rats previously hydrated with 0.5% sodium chloride. The decrease in urine outflow was associated with a dose-dependent reduction in the concentration of urine Na+ and K+. Two opioid-like peptides: β-endorphin and D-alanine2 methionine enkephalinamide shared this morphine action. On a molar basis, β-endorphin was about 100 times more potent than morphine to cause an equivalent antidiuresis. Naloxone injected i.p. antagonized the response of centrally administered morphine or β-endorphin on urine formation and composition. In addition, (+)-methadone or dextrorphan injected into the cerebral ventricles were considerably less active than their corresponding stereoisomers. N-methyl morphine injected i.p. was completely inactive up to doses that caused signs of toxicity; however, when injected into the lateral cerebral ventricles, it produced a decrease in the urine outflow and a reduction in the concentration of urine electrolytes. The pattern of changes in urine electrolytes produced by morphine and surrogates as well as the opioid-like peptides was in marked contrast to that caused by the i.p. administration of vasopressin. Whereas the i.p. administration of antidiuretic hormone caused oliguria and a large increase in the urine concentration of Na+ and K+, all the opiates produced at comparable antidiuresis a marked reduction in urine electrolytes. Results suggest that the opiates and the opioid-like peptides selectively activate central opiate receptors to produce changes in urine formation and composition. Results are discussed in relation to probable central opiate mechanisms controlling the production and formation of urine.

AB - The intraventricular injection of 10 to 30 nmol of morphine, (-)-methadone or levorphanol caused a reduction in the volume of the urine output in rats previously hydrated with 0.5% sodium chloride. The decrease in urine outflow was associated with a dose-dependent reduction in the concentration of urine Na+ and K+. Two opioid-like peptides: β-endorphin and D-alanine2 methionine enkephalinamide shared this morphine action. On a molar basis, β-endorphin was about 100 times more potent than morphine to cause an equivalent antidiuresis. Naloxone injected i.p. antagonized the response of centrally administered morphine or β-endorphin on urine formation and composition. In addition, (+)-methadone or dextrorphan injected into the cerebral ventricles were considerably less active than their corresponding stereoisomers. N-methyl morphine injected i.p. was completely inactive up to doses that caused signs of toxicity; however, when injected into the lateral cerebral ventricles, it produced a decrease in the urine outflow and a reduction in the concentration of urine electrolytes. The pattern of changes in urine electrolytes produced by morphine and surrogates as well as the opioid-like peptides was in marked contrast to that caused by the i.p. administration of vasopressin. Whereas the i.p. administration of antidiuretic hormone caused oliguria and a large increase in the urine concentration of Na+ and K+, all the opiates produced at comparable antidiuresis a marked reduction in urine electrolytes. Results suggest that the opiates and the opioid-like peptides selectively activate central opiate receptors to produce changes in urine formation and composition. Results are discussed in relation to probable central opiate mechanisms controlling the production and formation of urine.

UR - http://www.scopus.com/inward/record.url?scp=0019466042&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0019466042&partnerID=8YFLogxK

M3 - Article

VL - 217

SP - 579

EP - 585

JO - Journal of Pharmacology and Experimental Therapeutics

T2 - Journal of Pharmacology and Experimental Therapeutics

JF - Journal of Pharmacology and Experimental Therapeutics

SN - 0022-3565

IS - 3

ER -