Inhibition of prostate efferent neurotrasmission by amikacin

BACKGROUND: It has been suggested that manipulation of the autonomic nerve supply to the prostate leads to loss of functional and structural integrity of the gland, and that these changes may be useful in treating prostatic diseases. This study investigates the effect of amikacin on prostate efferent neurotransmission in vitro, in both rat and human prostate samples. METHODS: Prostate samples, obtained from male Wistar rats and 8 patients undergoing endoscopic surgery for benign prostatic hyperplasia, were studied by measurement of isometric contraction induced by electrical field stimulation (EFS), noradrenalin, carbachol, serotonin and ATP, in the presence or absence of amikacin 10(-3) M in a low-Ca medium. RESULTS: Amikacin significantly reduced EFS-induced contraction of isolated rat and human prostate samples by 45 +/- 6.5% (P < 0.01) and 47 +/- 6% (P < 0.01), respectively. Contraction was restored after addition of calcium chloride 2 x 10(-3) M. Amikacin-induced relaxation in rat prostate samples was greater than the effect of magnesium and weaker than those of prazosin and verapamil, but comparable in extent with the latter. No significant effect was observed on rat prostate contractile response to noradrenaline as to ATP in the presence of amikacin. Rat prostate contraction to carbachol and serotonin was inhibited by 35 +/- 11% (P < 0.05) and 59 +/- 11.7% (P < 0.01), respectively, after addition of amikacin 10(-3) M. CONCLUSIONS: Amikacin reduces in vitro both rat and human prostate contraction elicited by pre-junctional stimulation, but does not affect prostate contraction evoked by post-junctional stimulation. Our results indicate that amikacin affects prostatic efferent neurotransmission.