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Prostate Research Co-operative, Victorian College of Pharmacy, Monash University, 381 Royal Parade, Parkville, Victoria 3052, Australia ¹ Prince Henry's Institute of Medical Research, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria 3168, Australia

(Correspondence should be addressed to S Ventura; Email: sab.ventura{at}vcp.monash.edu.au)

This investigation aimed to see whether a change in the oestrogen to androgen ratio alters prostate contractility. Isolated organ bath studies using prostates from aromatase knockout (ArKO) mice which were homozygous (ArKO–/–) and heterozygous (ArKO+/–) for the disrupted aromatase cyp19 gene and wild-type littermates (ArKO+/+) were conducted. The distribution of noradrenergic nerves was visualized using the sucrose–potassium phosphate–glyoxylic acid method. ArKO–/– mice had increased prostate weights compared with ArKO+/+ mice. Frequency–response curves to electrical field stimulation (EFS; 0.5 ms pulse duration, 60 V, 0.1–20 Hz) yielded frequency-dependent contractions, while noradrenaline (10 nM–1 mM) and tyramine (1 µM–1 mM) produced concentration-dependent contractions. Prazosin (0.3 µM) attenuated the responses induced by noradrenaline and EFS in all mice (P0.019, n=5–7), while cocaine (10 µM) attenuated the responses evoked by tyramine (P<0.001, n=6). There were no genotype differences in EFS- and noradrenaline-induced responses (P0.506, n=10–13). Prostates from ArKO–/– and ArKO+/– mice were more sensitive to tyramine than prostates from ArKO+/+ mice (P<0.001, n=11–13). Dense adrenergic innervation of the prostate was similar in all mice. These results suggest that although the absence of aromatase increases prostatic growth, this translates only to a subtle and selective increase in contractility in mature mice.