Vasopressin modulates cerebrovascular responses to opioids in newborn pigs

W. M. Armstead, R. Mirro, S. L. Zuckerman, Charles Leffler

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Vasopressin receptor blockade has been observed to attenuate the systemic vascular effects of dynorphin. This study was designed to determine the ability of vasopressin to modulate cerebrovascular responses to opioids in newborn pigs equipped with closed cranial windows. Topical dynorphin 13 increased pial arteriolar diameter during normotension (151 ± 5, 171 ± 4, 183 ± 4 and 187 ± 4 μm for control, 10-10, 10-8 and 10-6 M dynorphin 13, respectively). During hypotension, however, responses to dynorphin 13 were reversed to concentration-dependent decreases in pial arteriolar diameter (184 ± 3, 169 ± 4, 165 ± 4 and 159 ± 4 μm for control 10-10, 10-8 and 10-6 M dynorphin 13, respectively). Dynorphin 13-induced pial arteriolar dilation was potentiated by the V1 receptor antagonist [1-(β-mercapto-ββ-cyclopentamethylene propionic acid) 2(o- methyl)-Tyr-AVP] (MEAVP; 5 μg/kg i.v.; 14 ± 1, 22 ± 1 and 24 ± 1% vs. 19 ± 1, 26 ± 1 and 30 ± 1% increase for 10-10, 10-8 and 10-6 M dynorphin 13 before and after MEAVP, respectively). In contrast, dynorphin 13-induced constriction during hypotension was markedly reduced by MEAVP (10 ± 1, 15 ± 1 and 16 ± 2% vs. 1 ± 1, 4 ± 1 and 9 ± 1% decrease for 10- 10, 10-8 and 10-6 dynorphin 13 before and after MEAVP, respectively). Dynorphin 8 and the synthetic κ-opioid selective agonist, U5O,488H, elicited similar tone-dependent responses that were modified by MEAVP in a similar fashion. β-Endorphin, a purported ε-opioid receptor agonist, produced vasoconstriction that was also inhibited by MEAVP. In contrast, methionine enkephalin- and leucine enkephalin-induced dilations were unchanged by MEAVP. These data indicate that vasopressin attenuates κ-opioid receptor-mediated dilation but contributes to constriction that can also be induced by activation of the same receptor. Furthermore, vasopressin also contributes to vasoconstriction induced by activation of the ε-receptor.

Original languageEnglish (US)
Pages (from-to)1107-1112
Number of pages6
JournalJournal of Pharmacology and Experimental Therapeutics
Volume260
Issue number3
StatePublished - Jan 1 1992

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Dynorphins
Vasopressins
Opioid Analgesics
Swine
Dilatation
Vasopressin Receptors
Opioid Receptors
Vasoconstriction
Constriction
Hypotension
Endorphins
Leucine Enkephalin
Methionine Enkephalin
Blood Vessels

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Pharmacology

Cite this

Vasopressin modulates cerebrovascular responses to opioids in newborn pigs. / Armstead, W. M.; Mirro, R.; Zuckerman, S. L.; Leffler, Charles.

In: Journal of Pharmacology and Experimental Therapeutics, Vol. 260, No. 3, 01.01.1992, p. 1107-1112.

Research output: Contribution to journalArticle

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abstract = "Vasopressin receptor blockade has been observed to attenuate the systemic vascular effects of dynorphin. This study was designed to determine the ability of vasopressin to modulate cerebrovascular responses to opioids in newborn pigs equipped with closed cranial windows. Topical dynorphin 13 increased pial arteriolar diameter during normotension (151 ± 5, 171 ± 4, 183 ± 4 and 187 ± 4 μm for control, 10-10, 10-8 and 10-6 M dynorphin 13, respectively). During hypotension, however, responses to dynorphin 13 were reversed to concentration-dependent decreases in pial arteriolar diameter (184 ± 3, 169 ± 4, 165 ± 4 and 159 ± 4 μm for control 10-10, 10-8 and 10-6 M dynorphin 13, respectively). Dynorphin 13-induced pial arteriolar dilation was potentiated by the V1 receptor antagonist [1-(β-mercapto-ββ-cyclopentamethylene propionic acid) 2(o- methyl)-Tyr-AVP] (MEAVP; 5 μg/kg i.v.; 14 ± 1, 22 ± 1 and 24 ± 1{\%} vs. 19 ± 1, 26 ± 1 and 30 ± 1{\%} increase for 10-10, 10-8 and 10-6 M dynorphin 13 before and after MEAVP, respectively). In contrast, dynorphin 13-induced constriction during hypotension was markedly reduced by MEAVP (10 ± 1, 15 ± 1 and 16 ± 2{\%} vs. 1 ± 1, 4 ± 1 and 9 ± 1{\%} decrease for 10- 10, 10-8 and 10-6 dynorphin 13 before and after MEAVP, respectively). Dynorphin 8 and the synthetic κ-opioid selective agonist, U5O,488H, elicited similar tone-dependent responses that were modified by MEAVP in a similar fashion. β-Endorphin, a purported ε-opioid receptor agonist, produced vasoconstriction that was also inhibited by MEAVP. In contrast, methionine enkephalin- and leucine enkephalin-induced dilations were unchanged by MEAVP. These data indicate that vasopressin attenuates κ-opioid receptor-mediated dilation but contributes to constriction that can also be induced by activation of the same receptor. Furthermore, vasopressin also contributes to vasoconstriction induced by activation of the ε-receptor.",
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N2 - Vasopressin receptor blockade has been observed to attenuate the systemic vascular effects of dynorphin. This study was designed to determine the ability of vasopressin to modulate cerebrovascular responses to opioids in newborn pigs equipped with closed cranial windows. Topical dynorphin 13 increased pial arteriolar diameter during normotension (151 ± 5, 171 ± 4, 183 ± 4 and 187 ± 4 μm for control, 10-10, 10-8 and 10-6 M dynorphin 13, respectively). During hypotension, however, responses to dynorphin 13 were reversed to concentration-dependent decreases in pial arteriolar diameter (184 ± 3, 169 ± 4, 165 ± 4 and 159 ± 4 μm for control 10-10, 10-8 and 10-6 M dynorphin 13, respectively). Dynorphin 13-induced pial arteriolar dilation was potentiated by the V1 receptor antagonist [1-(β-mercapto-ββ-cyclopentamethylene propionic acid) 2(o- methyl)-Tyr-AVP] (MEAVP; 5 μg/kg i.v.; 14 ± 1, 22 ± 1 and 24 ± 1% vs. 19 ± 1, 26 ± 1 and 30 ± 1% increase for 10-10, 10-8 and 10-6 M dynorphin 13 before and after MEAVP, respectively). In contrast, dynorphin 13-induced constriction during hypotension was markedly reduced by MEAVP (10 ± 1, 15 ± 1 and 16 ± 2% vs. 1 ± 1, 4 ± 1 and 9 ± 1% decrease for 10- 10, 10-8 and 10-6 dynorphin 13 before and after MEAVP, respectively). Dynorphin 8 and the synthetic κ-opioid selective agonist, U5O,488H, elicited similar tone-dependent responses that were modified by MEAVP in a similar fashion. β-Endorphin, a purported ε-opioid receptor agonist, produced vasoconstriction that was also inhibited by MEAVP. In contrast, methionine enkephalin- and leucine enkephalin-induced dilations were unchanged by MEAVP. These data indicate that vasopressin attenuates κ-opioid receptor-mediated dilation but contributes to constriction that can also be induced by activation of the same receptor. Furthermore, vasopressin also contributes to vasoconstriction induced by activation of the ε-receptor.

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