The effects on penile volume of nerve stimulations and drugs injected into the systemic circulation were studied plethysmographically. Dilator responses at selective perfusion of the penile artery were studied by measuring the perfusion pressure. The main results and conclusions are: The penis has an adrenergic vasoconstrictor supply coming from the sacrococcygeal parts of the sympathetic chains. A very low (0.2 Hz) vasomotor tone keeps the penis relaxed. If this tone is interrupted the penis will protrude but autoregulation will soon take over and eventually produce hyperinvolution of the penis. Two vasodilator paths, both with pelvic ganglionic relays, were found. 1) The pelvic parasympathetic nerves, probably having mainly non-cholinergic postganglionic neurons and operating quite effectively at low frequencies. 2) The sympathetic hypogastric nerves, presumably having at least partly cholinergic postganglionic neurons which, apart from muscarinic dilation of minute inflow resistance vessels to the erectile tissue, may also work by suppression of excitatory adrenergic neurotransmission. The pelvic and hypogastric vasodilator outflows work synergistically. The vasoconstrictor nerves are very strong and efficient antagonists of the vasodilator nerves.

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Glial cell line-derived neurotrophic factor (GDNF), a member of the GDNF family of neurotrophic factors, promotes the survival and function of several neuronal populations in the peripheral and central nervous system. In the present study, expression of GDNF mRNA in the shaft of adult rat penis is demonstrated. In situ hybridization revealed GDNF mRNA expression in cells lying in the narrow zone between the tunica albuginea and the cavernous tissue. Most subtunical cells exhibited immunoreactivity for vimentin and S100 beta, but they did not stain for smooth muscle alpha actin or PGP9.5. This suggests that the GDNF mRNA-expressing cells may have a mesenchymal origin. Also retrograde axonal transport of intracavernously injected 125I-labeled GDNF in penile parasympathetic and sensory neurons is shown. The transport was inhibited by excess unlabeled GDNF, whereas excess cytochrome c had no effect. This is in agreement with the view that the transport was mediated by binding to specific receptors located on axon terminals. In addition, this study demonstrates expression of GDNF family receptor-alpha 3 (GFR alpha 3) mRNA in most adrenergic, but only in a minor part (5.3%) of the penis-projecting adult rat major pelvic ganglion neurons, as well as in almost half (45.6%) of the penile S1 dorsal root ganglion neurons. In conclusion, the present data suggest that GDNF may act as a neurotrophic factor for subpopulations of adult rat penile parasympathetic and sensory neurons.