Objectives: To detect changes in growth hormone (GH) serum levels during different penile conditions in the cavernous and systemic blood of patients with erectile dysfunction and compare them with the course of GH registered in healthy men. It has been suggested that human GH is involved in sexual maturation and plays a regulatory role in male reproductive function. Deficiency may result in fatigability, loss of sexual desire and erection, or oligospermia or azoospermia. It is assumed that the biologic effects of GH include insulin-like growth factor 1-mediated stimulation of endothelial nitric oxide formation. It has recently been demonstrated that GH serum levels in the systemic and cavernous blood of healthy men increases during developing penile erection.
Methods: Thirty-five healthy adult men and 45 patients with erectile dysfunction of either organogenic or psychogenic etiology were exposed to visual and tactile erotic stimuli to elicit penile tumescence and, in the group of healthy subjects, rigidity. Whole blood was simultaneously aspirated from the corpus cavernosum and the cubital vein during the different functional conditions of the penis. Serum levels of GH were determined by means of an immunoradiometric assay.
Results: In the healthy subjects, systemic GH serum levels significantly increased during penile tumescence, followed by a transient decline from tumescence to rigidity and detumescence. In the unselected patients, the mean GH levels during penile flaccidity were determined to be about sevenfold lower than those registered in the blood of the healthy men. During penile tumescence, the mean increase in the GH levels in the systemic and cavernous blood of psychogenic patients was comparable to that seen in healthy men, but, in the group of organogenic patients, this increase was found to be negligible.
Conclusions: We believe our data provide strong evidence that GH may be of major importance in the maintenance of male erectile capability-probably through a stimulating effect on cyclic guanosine monophosphate generation in human cavernous smooth muscle-and that a decline in GH release may contribute to the manifestation of erectile dysfunction.