The HGN in female rats contained nerve endings that released nitric oxide (NO) and norepinephrine (NE). NO released during HGN stimulation inhibited the release of (NE) and reduced urethral infusion pressure in female rats. Nerves with synapses in the pelvic ganglia released NE in both male and female rats, but nerves that released NO did not have synapses in the ganglia. Only NE was released from the HGN nerve endings in male rats.

We simultaneously recorded the prostatic contractile and urethral pressure responses to electrical stimulation (ES) of the hypogastric nerves (HGNs) or phenylephrine in anesthetized rats and studied the effects of tamsulosin on these responses. At 0.01 and 0.1 mg/kg, i.v., tamsulosin inhibited the prostatic responses to ES of the HGNs in a dose-dependent manner, while at 1 microg/kg, i.v., it reduced the response to phenylephrine (0.01 mg/kg, i.v.) to about 26% of the nonantagonized level. These inhibitory effects on prostatic responses were maintained for 60 min. Tamsulosin exerted an inhibitory effect on the urethral response to ES of the HGNs at 0.01 mg/kg, i.v. but not at 0.1 mg/kg, i.v. At 1 microg/kg, i.v., tamsulosin also reduced the urethral response to phenylephrine to about 46% of the nonantagonized level; this effect was maintained for 60 min. Furthermore, tamsulosin was found to exert a stronger inhibitory effect on the prostatic response than on the urethral response induced by sympathetic nerve activation. Our findings suggest that rat urethral sympathetic nerve terminals may contain prejunctional alpha1 adrenoceptors that modulate the release of norepinephrine.

In the sensory branch of the PN, the nerves innervating the smooth muscles in the urethral sphincter were contained. In male rats norepinephrine mediates the UP elevation, but the neurotransmitter that mediates the UP reduction in female rats is not known.

The effects of KRN2391 (N-cyano-N'-(nitroxyethyl)-3-pyridine carboximidamide methane-sulfonate), which possesses ATP-sensitive potassium (K+) channel opening (KCO) activity and nitrate activity; Ki1769 (N-cyano-N'-(phenylethyl)-3-pyridinecarboximidamide methanesulfonate), which possesses only KCO activity; and nitroglycerin (NG) were determined on the motility of the ureter, urinary bladder and urethra of rats. Bladder contraction was induced by infusion of fluid into the bladder of conscious rats and recorded on a cystometrogram. KRN2391 and Ki1769 (both 0.3 mg/kg, i.v.) prolonged the micturition interval immediately after the injection, but NG (5 mg/kg, i.v.) did not. Peristaltic movement of the ureter, recorded in anesthetized rats, was inhibited by i.v. injection of KRN2391 and Ki1769 (both 0.03 mg/kg). However, when NG, NaNO2, N-nitro L-arginine methylester and methylene blue were applied directly to the ureter, no change in movement of the ureter was detected. KRN2391 (0.03 mg/kg, i.v.) and Ki1769 (0.3 mg/kg, i.v.) reduced the resistance to fluid infusion through the urethral lumen in anesthetized rats, whereas NG (0.5 mg/kg, i.v.) only reduced this resistance transiently. These results indicate that KCO activity had an inhibitory effect on the motility of the ureter, bladder and urethra. On the other hand, nitrate activity had an inhibitory effect on urethral tonus, corresponding to that induced by KCO activity.

The HGN in female rats contained nerve endings that released nitric oxide (NO) and norepinephrine (NE). NO released during HGN stimulation inhibited the release of (NE) and reduced urethral infusion pressure in female rats. Nerves with synapses in the pelvic ganglia released NE in both male and female rats, but nerves that released NO did not have synapses in the ganglia. Only NE was released from the HGN nerve endings in male rats.