Is there a peripheral site of action contributing to the voiding effects of α2-adrenoceptor agonists and antagonists?

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Standard

Is there a peripheral site of action contributing to the voiding effects of α2-adrenoceptor agonists and antagonists? / Aro, Erik; Bastman, Sanna; Andersson, Karl Erik; Streng, Tomi.

In: World Journal of Urology, Vol. 33, No. 3, 2015, p. 433-440.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Harvard

APA

CBE

MLA

Vancouver

Author

Aro, Erik ; Bastman, Sanna ; Andersson, Karl Erik ; Streng, Tomi. / Is there a peripheral site of action contributing to the voiding effects of α2-adrenoceptor agonists and antagonists?. In: World Journal of Urology. 2015 ; Vol. 33, No. 3. pp. 433-440.

Bibtex

@article{8c984131ded84755afd875e2da595cfc,
title = "Is there a peripheral site of action contributing to the voiding effects of α2-adrenoceptor agonists and antagonists?",
abstract = "Purpose Since it has not been established whether there is an effect on voiding exerted by direct stimulation or blockade of α2-adrenoceptors in the bladder and urethra, MK-467, a peripherally acting α2-adrenoceptor antagonist not penetrating into the CNS, was used to test whether part of the voiding effects of systemically given α2-adrenoceptor agonists is peripheral. Methods Urodynamic recordings from 27 conscious male adult C57/Bl J-strain mice were performed. After vehicle (saline) administration, two groups of animals were treated first with the selective α2-adrenoceptor agonist dexmedetomidine (Dex) and then with the selective α2-adrenoceptor antagonists atipamezole (Ati) or MK-467. Two other groups were first treated with Ati or MK-467 and then with Dex. Results Treatment with vehicle or α2-adrenoceptor antagonists alone did not affect micturition parameters. All animals treated first with Dex-developed overflow incontinence. Treatment with Ati after Dex reversed almost totally the effects of Dex on all voiding parameters, but treatment with MK-467 after Dex showed no detectable improvement. Treatment with Dex after Ati had no effect on any voiding parameter except maximal pressure. When mice were treated with Dex after MK-467, overflow incontinence was produced in seven of eight animals studied. Conclusions The absence of functionally relevant peripheral effects on voiding mediated via α2-adrenoceptors is supported by the finding that neither Ati nor MK-467 alone had any effect on micturition parameters and by the inability of MK-467 to inhibit the effects of Dex, suggesting that the relevant Dex effects were exerted within the CNS.",
keywords = "α-Adrenoceptors, Cystometry, Micturition, Peripheral action",
author = "Erik Aro and Sanna Bastman and Andersson, {Karl Erik} and Tomi Streng",
year = "2015",
doi = "10.1007/s00345-014-1336-z",
language = "English",
volume = "33",
pages = "433--440",
journal = "World Journal of Urology",
issn = "0724-4983",
publisher = "Springer",
number = "3",

}

RIS

TY - JOUR

T1 - Is there a peripheral site of action contributing to the voiding effects of α2-adrenoceptor agonists and antagonists?

AU - Aro, Erik

AU - Bastman, Sanna

AU - Andersson, Karl Erik

AU - Streng, Tomi

PY - 2015

Y1 - 2015

N2 - Purpose Since it has not been established whether there is an effect on voiding exerted by direct stimulation or blockade of α2-adrenoceptors in the bladder and urethra, MK-467, a peripherally acting α2-adrenoceptor antagonist not penetrating into the CNS, was used to test whether part of the voiding effects of systemically given α2-adrenoceptor agonists is peripheral. Methods Urodynamic recordings from 27 conscious male adult C57/Bl J-strain mice were performed. After vehicle (saline) administration, two groups of animals were treated first with the selective α2-adrenoceptor agonist dexmedetomidine (Dex) and then with the selective α2-adrenoceptor antagonists atipamezole (Ati) or MK-467. Two other groups were first treated with Ati or MK-467 and then with Dex. Results Treatment with vehicle or α2-adrenoceptor antagonists alone did not affect micturition parameters. All animals treated first with Dex-developed overflow incontinence. Treatment with Ati after Dex reversed almost totally the effects of Dex on all voiding parameters, but treatment with MK-467 after Dex showed no detectable improvement. Treatment with Dex after Ati had no effect on any voiding parameter except maximal pressure. When mice were treated with Dex after MK-467, overflow incontinence was produced in seven of eight animals studied. Conclusions The absence of functionally relevant peripheral effects on voiding mediated via α2-adrenoceptors is supported by the finding that neither Ati nor MK-467 alone had any effect on micturition parameters and by the inability of MK-467 to inhibit the effects of Dex, suggesting that the relevant Dex effects were exerted within the CNS.

AB - Purpose Since it has not been established whether there is an effect on voiding exerted by direct stimulation or blockade of α2-adrenoceptors in the bladder and urethra, MK-467, a peripherally acting α2-adrenoceptor antagonist not penetrating into the CNS, was used to test whether part of the voiding effects of systemically given α2-adrenoceptor agonists is peripheral. Methods Urodynamic recordings from 27 conscious male adult C57/Bl J-strain mice were performed. After vehicle (saline) administration, two groups of animals were treated first with the selective α2-adrenoceptor agonist dexmedetomidine (Dex) and then with the selective α2-adrenoceptor antagonists atipamezole (Ati) or MK-467. Two other groups were first treated with Ati or MK-467 and then with Dex. Results Treatment with vehicle or α2-adrenoceptor antagonists alone did not affect micturition parameters. All animals treated first with Dex-developed overflow incontinence. Treatment with Ati after Dex reversed almost totally the effects of Dex on all voiding parameters, but treatment with MK-467 after Dex showed no detectable improvement. Treatment with Dex after Ati had no effect on any voiding parameter except maximal pressure. When mice were treated with Dex after MK-467, overflow incontinence was produced in seven of eight animals studied. Conclusions The absence of functionally relevant peripheral effects on voiding mediated via α2-adrenoceptors is supported by the finding that neither Ati nor MK-467 alone had any effect on micturition parameters and by the inability of MK-467 to inhibit the effects of Dex, suggesting that the relevant Dex effects were exerted within the CNS.

KW - α-Adrenoceptors

KW - Cystometry

KW - Micturition

KW - Peripheral action

U2 - 10.1007/s00345-014-1336-z

DO - 10.1007/s00345-014-1336-z

M3 - Journal article

VL - 33

SP - 433

EP - 440

JO - World Journal of Urology

JF - World Journal of Urology

SN - 0724-4983

IS - 3

ER -