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Related Experiment Videos

Dopamine receptor subtypes that induce hyperactive urinary bladder response in anesthetized rats.

H Kontani1, T Inoue, T Sakai

  • 1Department of Pharmacology, Hokuriku University, School of Pharmacy, Kanazawa, Japan.

Japanese Journal of Pharmacology
|December 1, 1990
PubMed
Summary

Bromocriptine (BR) and SKF 38393 combination induced a hyperactive bladder response (HBR) in rats, mediated by D-2 receptors. D-1 receptor stimulation potentiated these D-2 agonist effects.

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Area of Science:

  • Pharmacology
  • Neuroscience
  • Urology

Background:

  • Dopamine receptors (D-1 and D-2) play roles in regulating various physiological functions.
  • The specific role of dopamine receptor subtypes in urinary bladder motility remains incompletely understood.

Purpose of the Study:

  • To investigate the effects of dopamine receptor agonists and antagonists on urinary bladder motility in anesthetized rats.
  • To elucidate the involvement of D-1 and D-2 dopamine receptors in mediating bladder responses.

Main Methods:

  • Administration of SKF 38393 (D-1 agonist), bromocriptine (BR, D-2 agonist), and their combinations intravenously in anesthetized rats.
  • Administration of dopamine receptor antagonists (SCH 23390, sulpiride, haloperidol) to assess their effects on induced bladder responses.

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  • Monitoring and recording of urinary bladder motility and responses.

    • Main Results:

    • SKF 38393 alone did not affect bladder motility.
    • Bromocriptine (BR) alone and in combination with SKF 38393 induced a hyperactive bladder response (HBR).
    • SCH 23390, sulpiride, and haloperidol suppressed the HBR induced by BR or BR + SKF 38393.

    Conclusions:

    • Hyperactive bladder response (HBR) is mediated by the activation of D-2 dopamine receptors.
    • Simultaneous stimulation of D-1 receptors potentiates the effects of D-2 agonists on bladder motility.
    • Dopamine receptor modulation offers a potential target for managing bladder dysfunction.