OBJECTIVES: To examine and compare the courses of norepinephrine (NE) and epinephrine (E) plasma levels in the systemic and cavernous blood taken during different penile conditions from healthy men and a group of patients with erectile dysfunction (ED). Knowledge concerning the neurophysiology of penile erection has improved tremendously during the past two decades. However, only few in vivo studies on human peripheral neurotransmission have been carried out to date. METHODS: Fifty-three healthy adult male subjects and 47 patients with ED of different etiologies were exposed to 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 different penile conditions. Plasma levels of NE and E were determined by means of a radioimmunoassay. RESULTS: In the healthy subjects, a significant reduction of NE in cavernous plasma was detected from flaccidity (362 +/- 173 pg/mL) to rigidity (248 +/- 122 pg/mL), followed by an increase in the detumescence phase (336 +/- 199 pg/mL). Changes in NE levels in the peripheral plasma were less pronounced. Cavernous E levels significantly increased from flaccidity (47 +/- 41 pg/mL) to tumescence (130 +/- 106 pg/mL) and dropped from rigidity (113 +/- 67 pg/mL) to detumescence (76 +/- 57 pg/mL). The course of systemic E plasma levels was similar to that in the cavernous blood. In contrast, median NE levels in the systemic and cavernous blood of the ED group slightly increased from flaccidity to tumescence (from 199 +/- 88 pg/mL to 210 +/- 99 pg/mL and from 273 +/- 140 pg/mL to 278 +/- 118 pg/mL, respectively). CONCLUSIONS: In healthy men, penile erection is accompanied by a reduction of NE in the cavernous blood and a rise in E levels in the peripheral and cavernous blood. That NE levels in the cavernous and systemic blood increase during sexual arousal in patients with ED might be an indication of a somatic dysregulation in sympathetic transmission or alterations of NE reuptake mechanisms as a cause of impaired erectile function.
OBJECTIVES: To examine and compare the courses of norepinephrine (NE) and epinephrine (E) plasma levels in the systemic and cavernous blood taken during different penile conditions from healthy men and a group of patients with erectile dysfunction (ED). Knowledge concerning the neurophysiology of penile erection has improved tremendously during the past two decades. However, only few in vivo studies on human peripheral neurotransmission have been carried out to date. METHODS: Fifty-three healthy adult male subjects and 47 patients with ED of different etiologies were exposed to 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 different penile conditions. Plasma levels of NE and E were determined by means of a radioimmunoassay. RESULTS: In the healthy subjects, a significant reduction of NE in cavernous plasma was detected from flaccidity (362 +/- 173 pg/mL) to rigidity (248 +/- 122 pg/mL), followed by an increase in the detumescence phase (336 +/- 199 pg/mL). Changes in NE levels in the peripheral plasma were less pronounced. Cavernous E levels significantly increased from flaccidity (47 +/- 41 pg/mL) to tumescence (130 +/- 106 pg/mL) and dropped from rigidity (113 +/- 67 pg/mL) to detumescence (76 +/- 57 pg/mL). The course of systemic E plasma levels was similar to that in the cavernous blood. In contrast, median NE levels in the systemic and cavernous blood of the ED group slightly increased from flaccidity to tumescence (from 199 +/- 88 pg/mL to 210 +/- 99 pg/mL and from 273 +/- 140 pg/mL to 278 +/- 118 pg/mL, respectively). CONCLUSIONS: In healthy men, penile erection is accompanied by a reduction of NE in the cavernous blood and a rise in E levels in the peripheral and cavernous blood. That NE levels in the cavernous and systemic blood increase during sexual arousal in patients with ED might be an indication of a somatic dysregulation in sympathetic transmission or alterations of NE reuptake mechanisms as a cause of impaired erectile function.