We investigated the pharmacological effects of adenosine on canine penile erection in vivo. Intracavernous injection of adenosine induced a full erection, which was unaffected by hexamethonium and atropine. The erectile response induced by adenosine was augmented by intracavernous pretreatment with dipyridamole and markedly depressed by theophylline. The erectile response induced by cavernous nerve stimulation was also enhanced by dipyridamole and reduced by theophylline. The combination of acetylcholine and adenosine, when injected intracavernously, induced a full erection, and the effect of these drugs was not additive but synergistic. These results suggest that penile erection induced by adenosine is due to a direct relaxing effect on cavernous smooth muscle. We propose that adenosine plays a cooperative role with acetylcholine and also has a physiological role as a neuromodulator in canine penile erection. adenosine ; dipyridamole ; theophylline ; penile erection ; dog Adenosine and adenine nucleotides are known to be potent vasodilators in various vascular beds and they play a significant role in physiological functions and pathological states (Snyder 1985). The inhibitory effect of adenosine is selectively antagonized by theophylline at the site of the adenosine receptor (Hayashi et al. 1978) and is potentiated by dipyridamole, which inhibits adenosine uptake (Hayashi et al. 1985).Penile erection is mediated by three types of neurological control : adrenergic, cholinergic and non-adrenergic and non-cholinergic (NANC) systems (Saenz de Tejada et al. 1988a). Although it has been suggested that vasoactive intestinal polypeptide (VIP) is the neurotransmitter of NANC nerves in canine penile erection (Anderson et al. 1984), canine penile erection induced by cavernous nerve stimulation was not abolished, but modified by VIP-anitibody (Juenemann et al.

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Castrated dogs showed a slightly weak erectile response to cavernous nerve stimulation compared with normal dogs. Intracavernous injection of acetylcholine induced a dose-dependent increase of intracavernous pressure in normal dogs, however, there was almost no penile response in castrated dogs. Histological study showed a significant higher ratio of collagen tissue/smooth muscle in the corpus cavernosum of castrated dogs, but no difference in acetylcholine-esterase staining and the number of endothelial cells lining the sinusoidal spaces between castrated and normal dogs. These results indicate that the corpus cavernosum of castrated dogs nearly lost responsiveness to acetylcholine probably due to a high ratio of collagen/smooth muscle fibers and that there are different mechanisms for erectile response to nerve stimulation and intracavernous injection of acetylcholine.castration ; acetylcholine ; penile erection ; corpus cavernosumThe main mechanism of sexual dysfunction in castrated humans and animals has been attributed to loss of sexual arousal, which is dependent on the plasma testosterone level (Michael and Wilson 1974). However, the local effects of castration on the penis are still unclear and controversial. Muller et al. (1988) found a very weak penile erectile response to cavernous nerve stimulation in three castrated dogs. However, Lin et al. (1990) recently reported that castration may not affect penile erectile ability and that a slight reduction of maximal intracavernous pressure in castrated dog was attributed to the concomitant decrease of basal systemic blood pressure.In the present study, we investigated erectile responses to nerve stimulation and intracavernous injection of acetylcholine (ACh), histological changes in the penis, and plasma testosterone levels in castrated dogs in comparison with those of non castrated normal dogs.

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