Evidence for local neural modulation of sympathetic influences on the feline bladder

It is known that resting conditions of bladder volume and pressure influence the response of the cat bladder in situ to sympathetic nerve stimulation. We observed that this was also true when the bladder was decentralized by cutting the sacral spinal roots, the hypogastric nerves, and one sympathetic chain. Under these conditions, elevating intravesical pressure by means of a reservoir of large surface area connected to the bladder resulted in an enhancement of the beta‐adrenoceptor‐mediated dilatory component of the response to stimulation of either the sympathetic chain or the hypogastric nerves. In order to test whether this enhancement was the result of mechanical or end‐organ effects, the change in response to ia isoprenaline was also evaluated. Although the response to isoprenaline was modestly (2‐fold) increased at intravesical pressures of 20–30 cm H₂O, the increase in response to hypogastric nerve stimulation (8.5‐fold) was significantly greater. The increase in response to sympathetic chain stimulation was intermediate, but only one chain was stimulated. Thus, end‐organ or physical factors have some influence on the dilatory response. However, there must be another modulatory component that exerts an effect on the neurally mediated dilatation but not on that produced by isoprenaline. This modulation appears to be activated by bladder distension and to be directed at the nerves, either on their terminals or at the intramural or plexus ganglia. Candidate mechanisms are humoral compounds (e.g., eicosanoids) or a local neural network.