Pathways Involving Beta‐3 Adrenergic Receptors Modulate Cold Stress‐Induced Detrusor Overactivity in Conscious Rats

Imamura, Tetsuo; Ishizuka, Osamu; Ogawa, Toshihide; Yamagishi, Takahiro; Yokoyama, Hitoshi; Minagawa, Tomonori; Nakazawa, Masaki; Nishizawa, Osamu

doi:10.1111/luts.12050

Cited by 3 publications

(5 citation statements)

References 15 publications

(29 reference statements)

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“…Our previous study showed that the cold stress-induced bladder overactivity of Sprague-Dawley (SD) rats without any underlying disease was inhibited by treatments with 1.0 mg/kg CL316243, another β 3adrenergic receptor agonist. 19 Thus, we concluded that the cold stress-induced bladder overactivity in normal SD rats is mediated with pathways involving β 3 -adrenergic receptors. However, in the present study, the bladder overactivity of GK rats was not inhibited by treatments with either 0.1 mg/kg or 1.0 mg/kg mirabegron, even though expression of β 3 -adrenergic receptor mRNA and protein were detected within the urinary bladders.…”

Section: Discussionmentioning

confidence: 77%

“…Our previous study showed that the cold stress‐induced bladder overactivity of Sprague–Dawley (SD) rats without any underlying disease was inhibited by treatments with 1.0 mg/kg CL316243, another β 3 ‐adrenergic receptor agonist 19 . Thus, we concluded that the cold stress‐induced bladder overactivity in normal SD rats is mediated with pathways involving β 3 ‐adrenergic receptors.…”

Section: Discussionmentioning

confidence: 88%

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Cold stress‐induced bladder overactivity in type 2 diabetic mellitus rats is mitigated by the combination of a M₃‐muscarinic antagonist and a β₃‐adrenergic agonist

Hara

Imamura

Suzuki

et al. 2022

LUTS

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Objectives: Goto-Kakizaki (GK) rats with type 2 diabetes mellitus respond to low temperature (LT) environments with bladder overactivity, including increased voiding frequency and decreased voiding interval and micturition volume. We determined if bladder overactivity could be inhibited by treatment with the combination of a M 3 -muscarinic receptor antagonist and a β 3 -adrenergic receptor agonist.Methods: Ten-week-old female GK rats were fed a high-fat diet for 4 weeks. Cystometric investigations were conducted at room temperature (RT, 27 ± 2 C). The rats were then intraperitoneally administered the vehicle, the M 3 -muscarinic receptor antagonist solifenacin, the β 3 -adrenergic agonist mirabegron, or a combination of solifenacin and mirabegron. Ten minutes after the administrations, the rats were transferred to the LT environment (4 ± 2 C), where the cystometric measurements were continued. The expressions of both M 3 -muscarinic and β 3 -adrenergic receptors were investigated.Results: After transfer from RT to LT, both voiding interval and bladder capacity of the vehicle-, solifenacin-, or mirabegron-treated rats were significantly decreased.However, the combination of solifenacin and mirabegron significantly mitigated the bladder overactivity. While both M 3 -muscarinic and β 3 -adrenergic receptors were detected, the expression of M 3 -muscarinic receptor mRNA was significantly higher than that of β 3 -adrenergic receptor mRNA. Conclusions:The cold stress-induced bladder overactivity was not improved by either the M 3 -muscarinic receptor antagonist or the β 3 -adrenergic receptor agonist alone. However, the combined treatment mitigated the cold stress responses. Combined therapy with M 3 -muscarinic antagonists and β 3 -adrenergic agonists could reduce side effects and improve the quality of life for diabetic patients with bladder overactivity.

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Section: Discussionmentioning

confidence: 77%

Section: Discussionmentioning

confidence: 88%

Cold stress‐induced bladder overactivity in type 2 diabetic mellitus rats is mitigated by the combination of a M₃‐muscarinic antagonist and a β₃‐adrenergic agonist

Hara

Imamura

Suzuki

et al. 2022

LUTS

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“…We previously showed that the same low dose (0.1 mg/kg) of the β 3 ‐AR agonist CL316243 did not inhibit the cold stress‐induced responses in SD rats . However, a higher dose, 1.0 mg/kg, did inhibit the cold stress‐induced detrusor overactivity . Thus, we suggested that while the pathways involving β 3 ‐ARs could mediate the cold stress‐induced responses, the effects were dose dependent.…”

Section: Discussionmentioning

confidence: 80%

“…Similarly, treatment of the SHRs with mirabegron alone did not inhibit the cold stress‐induced detrusor overactivity patterns. We previously showed that the same low dose (0.1 mg/kg) of the β 3 ‐AR agonist CL316243 did not inhibit the cold stress‐induced responses in SD rats . However, a higher dose, 1.0 mg/kg, did inhibit the cold stress‐induced detrusor overactivity .…”

Section: Discussionmentioning

confidence: 94%

“…Previously, in Goto–Kakizaki (GK) rats, which serve as disease model for diabetes mellitus, we showed that the MR antagonist imidafenacin could inhibit the detrusor overactivity induced by sudden drops to low temperature (LT) . Similarly, a high dose (1.0 mg/kg) of the β 3 ‐AR agonist CL316243 could also inhibit the cold stress‐induced detrusor overactivity in healthy Sprague–Dawley (SD) rats . These results suggested that the M 3 ‐MRs and β 3 ‐ARs might partially mediate pathways of cold stress‐induced detrusor overactivity.…”

Section: Introductionmentioning

confidence: 88%

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Combined treatment with a β₃‐adrenergic receptor agonist and a muscarinic receptor antagonist inhibits detrusor overactivity induced by cold stress in spontaneously hypertensive rats

Imamura

Ogawa

Minagawa

et al. 2016

Neurourology and Urodynamics

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Aims: This study determined if combined treatment with the muscarinic receptor (MR) antagonist solifenacin and the b 3 -adrenergic receptor (AR) agonist mirabegron could inhibit detrusor overactivity induced by cold stress in spontaneously hypertensive rats (SHRs). Methods: Thirty-two female 10-week-old SHRs were fed an 8% NaCl-supplemented diet for 4 weeks. Cystometric measurements of the unanesthetized, unrestricted rats were performed at room temperature (RT, 27 AE 28C) for 20 min. The rats were then intravenously administered vehicle, 0.1 mg/kg solifenacin alone, 0.1 mg/kg mirabegron alone, or the combination of 0.1 mg/kg mirabegron and 0.1 mg/kg solifenacin (n ¼ 8 each group). Five minutes later, the treated rats were exposed to low temperature (LT, 4 AE 28C) for 40 min. Finally, the rats were returned to RT. After the cystometric investigations, the b 3 -ARs and M 3 -MRs expressed within the urinary bladders were analyzed. Results: Just after transfer from RT to LT, vehicle-, solifenacin-, and mirabegron-treated SHRs exhibited detrusor overactivity that significantly decreased voiding interval and bladder capacity. However, treatment with the combination of solifenacin and mirabegron partially inhibited the cold stressinduced detrusor overactivity patterns. The decreases of voiding interval and bladder capacity in the combination-treated rats were significantly inhibited compared to other groups. Within the urinary bladders, there were no differences between expression levels of M 3 -MR and b 3 -AR mRNA. The tissue distribution of M 3 -MRs was similar to that of the b 3 -ARs. Conclusions: This study suggested that the combination of solifenacin and mirabegron act synergistically to inhibit the cold stress-induced detrusor overactivity in SHRs. Neurourol.

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Efficacy of the combination of KPR-5714, a novel transient receptor potential melastatin 8 (TRPM8) antagonist, and β3-adrenoceptor agonist or anticholinergic agent on bladder dysfunction in rats with bladder overactivity

Aizawa

Fujimori

Nakanishi

et al. 2021

European Journal of Pharmacology

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Pathways Involving Beta‐3 Adrenergic Receptors Modulate Cold Stress‐Induced Detrusor Overactivity in Conscious Rats

Abstract: A high dose of the beta-3 agonist CL316243 could modulate cold stress-induced detrusor overactivity. Therefore, one of the mechanisms in cold stress-induced detrusor overactivity includes a pathway involving beta-3 ARs.

Cited by 3 publications

References 15 publications

Cold stress‐induced bladder overactivity in type 2 diabetic mellitus rats is mitigated by the combination of a M₃‐muscarinic antagonist and a β₃‐adrenergic agonist

Cold stress‐induced bladder overactivity in type 2 diabetic mellitus rats is mitigated by the combination of a M₃‐muscarinic antagonist and a β₃‐adrenergic agonist

Combined treatment with a β₃‐adrenergic receptor agonist and a muscarinic receptor antagonist inhibits detrusor overactivity induced by cold stress in spontaneously hypertensive rats

Efficacy of the combination of KPR-5714, a novel transient receptor potential melastatin 8 (TRPM8) antagonist, and β3-adrenoceptor agonist or anticholinergic agent on bladder dysfunction in rats with bladder overactivity

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Pathways Involving Beta‐3 Adrenergic Receptors Modulate Cold Stress‐Induced Detrusor Overactivity in Conscious Rats

Abstract: A high dose of the beta-3 agonist CL316243 could modulate cold stress-induced detrusor overactivity. Therefore, one of the mechanisms in cold stress-induced detrusor overactivity includes a pathway involving beta-3 ARs.

Cited by 3 publications

References 15 publications

Cold stress‐induced bladder overactivity in type 2 diabetic mellitus rats is mitigated by the combination of a M3‐muscarinic antagonist and a β3‐adrenergic agonist

Cold stress‐induced bladder overactivity in type 2 diabetic mellitus rats is mitigated by the combination of a M3‐muscarinic antagonist and a β3‐adrenergic agonist

Combined treatment with a β3‐adrenergic receptor agonist and a muscarinic receptor antagonist inhibits detrusor overactivity induced by cold stress in spontaneously hypertensive rats

Efficacy of the combination of KPR-5714, a novel transient receptor potential melastatin 8 (TRPM8) antagonist, and β3-adrenoceptor agonist or anticholinergic agent on bladder dysfunction in rats with bladder overactivity

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Cold stress‐induced bladder overactivity in type 2 diabetic mellitus rats is mitigated by the combination of a M₃‐muscarinic antagonist and a β₃‐adrenergic agonist

Cold stress‐induced bladder overactivity in type 2 diabetic mellitus rats is mitigated by the combination of a M₃‐muscarinic antagonist and a β₃‐adrenergic agonist

Combined treatment with a β₃‐adrenergic receptor agonist and a muscarinic receptor antagonist inhibits detrusor overactivity induced by cold stress in spontaneously hypertensive rats