Abstract
Intracerebroventricular morphine consistently inhibited spontaneous urinary bladder contractions recorded from the anesthetized rat. This effect was reversed by naloxone and appeared to be exerted within the forebrain. Neither dynorphin-(1-13) nor U-50, 488 (kappa-agonists) affected bladder motility. Ethylketocyclazocine inhibited contractions only at higher doses, possibly due to mu-receptor interactions. Bladder activity was consistently inhibited by the mu-agonists morphiceptin and [D-Ala2, MePhe4, Gly-(ol)5]enkephalin (DAGO) and by [D-Ala2, D-Leu5]enkephalin (DADLE, delta-agonist). DAGO was the most potent compound tested. These observations support the involvement of mu- and possibly delta-receptors in the centrally mediated inhibition of urinary bladder motility by opioids.
MeSH terms
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Animals
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Enkephalin, Ala(2)-MePhe(4)-Gly(5)-
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Enkephalin, Leucine / analogs & derivatives
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Enkephalin, Leucine / pharmacology
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Enkephalin, Leucine-2-Alanine
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Enkephalins / pharmacology
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Female
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In Vitro Techniques
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Injections, Intravenous
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Injections, Intraventricular
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Morphine / pharmacology
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Muscle Contraction / drug effects
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Naloxone / pharmacology
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Narcotics / pharmacology
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Rats
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Rats, Inbred Strains
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Receptors, Opioid / drug effects*
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Receptors, Opioid / metabolism
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Receptors, Opioid, delta
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Receptors, Opioid, kappa
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Receptors, Opioid, mu
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Urinary Bladder / drug effects*
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Urinary Bladder / physiology
Substances
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Enkephalins
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Narcotics
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Receptors, Opioid
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Receptors, Opioid, delta
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Receptors, Opioid, kappa
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Receptors, Opioid, mu
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Enkephalin, Ala(2)-MePhe(4)-Gly(5)-
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Naloxone
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Enkephalin, Leucine
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Enkephalin, Leucine-2-Alanine
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Morphine