INTRODUCTION

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.

MATERIALS AND METHODS

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.

RESULTS

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.

CONCLUSIONS

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.