CONTRACTILITY CHANGES OF THE DEEP DORSAL PENILE VEIN DUE TO SEROTONIN

Citation
Aa. Esen et al., CONTRACTILITY CHANGES OF THE DEEP DORSAL PENILE VEIN DUE TO SEROTONIN, The Journal of urology, 158(1), 1997, pp. 234-237
Citations number
17
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
00225347
Volume
158
Issue
1
Year of publication
1997
Pages
234 - 237
Database
ISI
SICI code
0022-5347(1997)158:1<234:CCOTDD>2.0.ZU;2-J
Abstract
Purpose: Penile erection is a complex neurovascular phenomenon that ta kes place with the active contribution of arterial and sinusoidal stru ctures. However, some authors claim that larger veins including the de ep dorsal veins that produce contractions, might be involved in the ph ysiology of erection. This study was designed to clarify the contracti le properties of deep dorsal penile veins (DDPV). Materials and Method s: The effect of serotonin (5-HT), noradrenaline (NA), adenosine triph osphate (ATP) and acethylcholine (Ach) on the isolated DDPVs of 16 imp otent men, 9 with veno-occlusive dysfunction and 7 without venous leak age, and 5 potent men (controls) who underwent radical prostatectomy, were examined in vitro. Results: Although NA, ATP and Ach had no effec t, 5-HT produced concentration-dependent contractions. E-max and pEC(5 0) of 5-HT were 411 +/- 10 mg., 5.92 +/- 0.25; 1020 +/- 260 mg., 5.83 +/- 0.24 and 160 +/- 40 mg., 6.4 +/- 0.22 in controls and patients who had venous leakage and no venous leakage, respectively. Samples of co ntrols were contracted only with 5-HT2 agonist, DOI (pEC(50) = 5.63 +/ - 0.02), and these contractions were antagonized with 5-HT2 antagonist ketanserin. On the other hand, both DOI (pEC(50) = 6.30 +/- 0.77) and 5-HT1 agonist, 5-HT (pEC(50) 6.23 +/- 0.21) produced venoconstriction in patients with veno-occlusive dysfunction. Conclusions: The present findings suggest that 5-HT receptor functions in the DDPVs are of 5-H T2 subtype in potent men and the altered response to 5-HT in patients with veno-occlusive disease may play a role in the pathophysiology of impotence.