Abstract
Overactive bladder (OAB), a symptom syndrome defined as urgency, is a common clinical condition, which sometimes cannot be satisfactorily treated with current medications in every subject; therefore, alternatives are needed. The aim of this in vitro study was to investigate the effects of ivabradine, a selective pacemaker If current inhibitor, on agonist-induced isometric contractions of the bladder smooth muscles. Urinary bladder strips were isolated from adult male Wistar rats and suspended in a tissue bath containing physiological solution. The strips were contracted by bath applications of carbachol (CCh, 1 μM). Ivabradine (30 μM, 60 μM or 90 μM) was added to the tissue bath either prior to or after the application of the agonist, and the resulting contractile activity was compared to the preceding contractile activity. The amplitude and area under force-time curves (AUFC) of the isometric contractions were evaluated. The addition of CCh caused a marked stimulation of contractile force in isolated urinary bladder strips, which was significantly inhibited by ivabradine, both in terms of peak amplitude (29% ±3%, 20% ±6% and 18% ±6% by 30 μM, 60 μM and 90 μM ivabradine, respectively) and AUFC (47% ±5.5%, 35% ±8% and 35% ±6% by 30 μM, 60 μM and 90 μM ivabradine, respectively; n = 7 for each). Pre-treatment with ivabradine (10 μM) significantly attenuated the contractile response to CCh (1 μM; mean peak amplitude from 1493 ±216 mg to 680 ±95 mg; p < 0.003; n = 7). The results of this in vitro study demonstrated that ivabradine inhibits cholinergic agonistinduced bladder contractions, which means that in the future ivabradine may be used in OAB treatment.
Highlights
The urinary bladder is a distensible, membranous, hollow organ, made of a thin layer of smooth muscle that provides its unique properties of relaxing to accommodate and contracting to empty out urine, one of the body’s continuously produced fluid waste products
The addition of CCh caused a marked stimulation of contractile force in isolated urinary bladder strips, which was significantly inhibited by ivabradine, both in terms of peak amplitude (29% ±3%, 20% ±6% and 18% ±6% by 30 μM, 60 μM and 90 μM ivabradine, respectively) and area under force-time curves (AUFC) (47% ±5.5%, 35% ±8% and 35% ±6% by 30 μM, 60 μM and 90 μM ivabradine, respectively; n = 7 for each)
The results of this in vitro study demonstrated that ivabradine inhibits cholinergic agonistinduced bladder contractions, which means that in the future ivabradine may be used in Overactive bladder (OAB) treatment
Summary
The urinary bladder is a distensible, membranous, hollow organ, made of a thin layer of smooth muscle that provides its unique properties of relaxing to accommodate and contracting to empty out urine, one of the body’s continuously produced fluid waste products. The detrusor can become too active and contract involuntarily, making the individual feel the urge to void inappropriately, even when the bladder has little urine This clinical symptom is referred to as overactive bladder (OAB), typically caused by spasms of the bladder muscles with or without incontinence.[5] Overactive bladder is a very common chronic condition that affects the daily lives of a huge number of men, women and children worldwide.[5,6] Urinary urgency, frequent urination and nocturia are a common set of OAB symptoms that can be caused by a wide range of conditions, including detrusor hyperreflexia, urinary tract infections and obstructive prostatic hypertrophy.[5,6] Whatever the underlying cause, intense and involuntary bladder muscle contractions are present. Overactive bladder (OAB), a symptom syndrome defined as urgency, is a common clinical condition, which sometimes cannot be satisfactorily treated with current medications in every subject; alternatives are needed
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