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Activation of beta3 adrenoreceptors decreases the amplitude of the electrical field stimulation induced contractions in rat detrusor smooth muscle isolated strips
Author(s) -
afeli serge amani yao,
petkov georgi v
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1115.18
Subject(s) - purinergic receptor , stimulation , agonist , endocrinology , cholinergic , chemistry , medicine , inhibitory postsynaptic potential , overactive bladder , detrusor muscle , carbachol , suramin , atropine , antagonist , urinary bladder , receptor , alternative medicine , pathology
It is believed that during bladder filling phase, β‐adrenoceptors (β‐AR) facilitate relaxation of the detrusor smooth muscle (DSM). Our previous studies showed that BRL37344, a specific β3‐AR agonist, caused a concentration‐dependant decrease in the myogenic contractions of rat isolated DSM strips. Here, using tissue baths equipped with electrodes for electrical field stimulation (EFS), we investigated the role of β3‐AR in rat DSM neurogenic contractions. Neurogenic contractions were generated by EFS pulses (20 V amplitude, 0.75 ms width, and 3 s duration) with increasing frequencies (0.5–50 Hz). BRL37344 (100 μM) significantly decreased the amplitude of the EFS‐induced contractions of rat DSM (n=12, N=6). We further used specific inhibitors to separate the cholinergic and purinergic components of the EFS‐induced contractions of rat DSM. The BRL37344 inhibitory effect was also observed in the presence of 1 μM atropine (n=15, N=8) as well as in the presence of 10 μM suramin and 10 μM α,β‐methylene‐ATP (n=13, N=5). BRL37344 (100 μM) inhibitory effect was blocked by SR59230A (10 μM), a specific β3‐AR antagonist (n=8, N=3). SR59230A per se did not have any effect on the neurogenic contractions (n=8, N=3). In conclusion, activation of β3‐AR decreases DSM neurogenic contractions, thus making β3‐AR a new pharmacological target for the treatment of overactive bladder.