L-carnitine treatment partially restores urinary bladder function of streptozotocin diabetic rats

Diabetes mellitus is associated with urinary bladder dysfunction. This study determined whether or not detrusor responses were altered and reversed by L-carnitine treatment in the urinary bladders of diabetic rats.

Three groups of animals were used: streptozotocin-treated (45 mg x kg(-1) i.p., 8 weeks), parallel L-carnitine-treated (0.6 g x kg(-1) x day(-1) i.p.), and control rats. Contractile and relaxant responses were measured using isolated bath techniques.

Serum glucose levels in diabetic rats were partially reversed after L-carnitine treatment. Detrusor strips from diabetic rats exhibited an increase in response to electrical field stimulation (EFS; 0.5-32 Hz). Treatment with L-carnitine restored the hyperreactivity to EFS-induced contractility. The response to direct activation of the smooth muscle with carbachol and KCl remained unaltered. In relaxation studies, the urinary bladders of diabetic rats displayed a diminished response to isoprenaline, an unchanged response to ATP, and an increased response to adenosine of the ATP metabolite. L-carnitine treatment restored the hyporesponsiveness of isoprenaline and the hyperresponsiveness of adenosine-elicited relaxation.

These findings show that carnitine can be implicated in the contractile response of noradrenergic noncholinergic nerve stimulation and the relaxation response of isoprenaline and adenosine. Hence, L-carnitine deficiency can contribute to voiding deficiency in diabetic patients.