Effect of low androgen status on the expression of adenosine A2A and A2B receptors in rat penile corpus cavernosum

To investigate whether low androgen status affects erectile function by regulating the expression of adenosine A_2A and A_2B receptors in rat penile corpus cavernosum. Thirty‐six 8‐week‐old male Sprague‐Dawley rats were randomly divided into six groups: sham‐operated group (4w‐sham, 8w‐sham), castration group (4w‐cast, 8w‐cast) and androgen replacement group (4w‐cast+T, 8w‐cast+T). The rats in the androgen replacement groups were subcutaneously injected with testosterone propionate (3 mg/kg) every other day after castration. The maximum intracavernous pressure/mean arterial pressure (ICPmax/MAP), the expression of A_2A, A_2B, AKT and eNOS and the concentrations of cAMP and cGMP in the corpus cavernosum were detected at the 4th and 8th weeks after the operation. The serum testosterone level and the ratio of ICPmax/MAP decreased significantly in the castration group as compared to other groups (p < 0.01). There was no significant difference in the expression of A_2A receptor among groups, while the expression of A_2B, AKT and eNOS and the concentrations of cAMP and cGMP in the castration group were significantly lower than in other groups (p < 0.01). Low androgen status inhibits the AKT/eNOS/cGMP signalling pathways and the production of cAMP in the corpus cavernosum of castrated rats by down‐regulating the expression of A_2B receptor, and results in decreased of ICPmax/MAP.     

Effect of low androgen levels on the sulphur dioxide signalling pathway in rat penile corpus cavernosum

The aim of this study was to investigate the relationship between sulphur dioxide (SO₂) signalling pathway and the changes in erectile function under low androgen levels. Thirty‐six healthy male Sprague Dawley (SD) rats aged eight weeks were randomly divided into androgen replacement group, castration group and sham group. Rats in the androgen replacement group were subcutaneously injected with testosterone propionate at 3 mg/kg every other day postcastration. The maximum intracavernous pressure/mean arterial pressure (ICP_max/MAP) and the relative content of SO₂ in the penile corpus cavernosum were measured. The mRNA and protein expressions of aspartate aminotransferase (AAT1 and AAT2), cysteine oxidase (CDO), endothelial nitric oxide synthase (eNOS) and phosphorylation of endothelial nitric oxide synthase (P‐eNOS) were detected. ICP_max/MAP, P‐eNOS/eNOS and the level of SO₂ decreased significantly in the castration group compared to the other groups (p < 0.05). The expressions of mRNA and protein decreased significantly in the castration group compared to the androgen replacement group and the sham group (p < 0.05), while there was no significant difference between the androgen replacement group and sham group. Low androgen levels can inhibit erectile function by downregulating the SO₂ signalling pathway.     

Rho激酶及血红素氧合酶在自发性高血压大鼠阴茎海绵体中的表达

目的:探讨NOS/NO、HO/CO、RhoA/Rho激酶等信号通路在自发性高血压大鼠(SHR)阴茎海绵体中的表达及相互关系。方法:健康成年雄性SPF级SHR与对照组WKY大鼠各7只,16周龄,体重250~300g。麻醉后颈动脉和海绵体内插管连续监测平均动脉压(MAP)和海绵体内压(ICP)。利用电刺激海绵体神经,记录ICP/MAP比值变化。利用免疫组化和Western印迹方法分析ROCK2、HO-2、eNOS在阴茎海绵体中的表达变化。结果:SHR组在利用电刺激海绵体神经后ICP/MAP比值升高不明显(P>0.05),海绵体组织中ROCK2蛋白表达水平升高显著(P=0.017),HO-2表达水平则降低显著(P=0.006)。HO-2主要位于阴茎海绵体的平滑肌细胞及神经细胞内,eNOS则主要位于阴茎海绵体血管内皮细胞,两者在SHR组表达明显降低。结论:NOS/NO、HO/CO、RhoA/Rho激酶与SHRED有关,并且可能互相影响。     

法舒地尔对高血压大鼠勃起功能的影响

目的:探讨Rho激酶抑制剂法舒地尔对高血压大鼠勃起功能的影响及其机制。方法:12周龄雄性SD大鼠随机分成对照组(A组)、高血压组(B组)、法舒地尔治疗组(C组),建立高血压大鼠模型后,C组给予法舒地尔[30 mg/(kg.d)]腹腔注射,A组、B组给予等量生理盐水腹腔注射,术后10周测量大鼠阴茎海绵体内压/平均颈动脉压(ICPmax/MAP),Western印迹法测定ROCK1、ROCK2蛋白在阴茎海绵体的表达水平。结果:B组收缩压(mmHg)、ROCK1、ROCK2蛋白表达(190.39±5.07、0.048±0.002、0.143±0.011)较A组(124.81±4.01、0.036±0.001、0.101±0.011)显著增加(P<0.05),C组收缩压(mmHg)、ROCK1、ROCK2蛋白表达(182.03±4.32、0.044±0.001、0.126±0.007)较B组显著降低(P<0.05),B组ICPmax/MAP(36.82±5.47)较A组(59.99±5.69)显著降低(P<0.05),C组(51.1±5.63)较B组显著提高(P<0.05)。结论:法舒地尔可通过抑制RhoA/Rho激酶信号高表达及可能的降血压作用而改善高血压大鼠勃起功能。     

血红素氧合酶2在去势大鼠阴茎海绵体内的表达

目的:研究去势大鼠阴茎海绵体血红素氧合酶2(HO-2)和内皮型一氧化氮合酶(eNOS)的表达,探讨雄激素与HO-2、eNOS在ED中的作用及相关性。方法:10周龄雄性SD大鼠40只,分为4、8、12周组和正常对照组各10只,实验组采取手术切除双侧睾丸,对照组采取假手术。分别于术后4、8、12周测定大鼠血清睾酮(T)、阴茎海绵体内压(ICP)、平均颈动脉压(MAP),取阴茎标本,采用Western印迹分析阴茎海绵体HO-2含量,免疫组化分析HO-2和eNOS的表达。结果:去势各组血清T水平较正常对照组显著下降(P<0.05)。经3V、5V电压刺激后去势各组ICP/MAP值明显下降(P<0.05)。HO-2在正常和去势大鼠阴茎海绵体组织均有表达,去势4周组HO-2光密度分布曲线下面积(341.50±99.70)较正常组(876±443.36)和去势8周组(705.00±152.74)明显下降(P<0.05),去势8周与正常组之间无显著变化(P>0.05),去势12周没有检测到HO-2的表达。eNOS主要表达于阴茎海绵体血管内皮细胞,去势组eNOS(123.94±30.23)较正常组(421.21±125.12)差异有显著性(P<0.05)。T与eNOS和HO-2表达呈高度正相关(r=0.976、0.946,P均<0.05)。结论:雄激素可能通过影响大鼠阴茎海绵体HO-2、eNOS的表达参与阴茎勃起功能调控。     

Effects of intracavernous injection of P2X3 and NK1 receptor antagonists on erectile dysfunction induced by spinal cord transection in rats

This study aimed to explore the effects of intracavernous injection (ICI) of P2X3 and NK1 receptor antagonists on erectile dysfunction (ED) induced by spinal cord transection in rats. Sixty male Sprague–Dawley (SD) rats were randomly divided into the following three groups (20 rats each group): sham operation group (C group), thoracic spinal cord transection group (T group) and sacral spinal cord transection group (S group). An ED model was established through complete transection of the thoracic or sacral spinal cord. Intracavernous pressure (ICP) with and without injection of P2X3 (Suramin) or NK1 (GR82334) receptor antagonists was recorded 3 weeks after surgery. Immunohistochemistry was employed to detect the expression of P2X3 and NK1 receptors in the dorsal root ganglion (DRG) and smooth muscle of corpus cavernosum. Data were processed with SPSS 17.0. ICI with Suramin (0.1, 0.3 and 1 mm ) or GR82334 (0.1, 0.3 and 1 mm ) increased ICP dose dependently in the T and S groups. The expression of P2X3 and NK1 receptors in DRG and smooth muscle of corpus cavernosum was up‐regulated in the T and S groups. It is concluded that ICI of P2X3 and NK1 receptor antagonists may improve the recovery of erectile function in a rat model with ED after spinal cord transection.     

Apoptosis in rat erectile tissue induced by castration

Aim: To investigate the effect of androgen on the structure of corpus cavemosum. Methods: Thirty- mature rats wererandomized into 3 groups, i.e., simple castration, castration with testosterone (T) supplementation and sham-operatedcontrots. One week after operation, the animals were sacrificed and corpora cavenosa harvested. Apoptosis was detect-ed with the in sita end labeling (1SEL) techniques and DNA fragment analysis. Results: The apoptotic rate was4.19 % in the simple castrated rats, 0.2 % in castrated rats supplemented with T and 0.14 % in the cona‘ols. Signifi -cant difference was found between the simple castrates and other two groups (P＜0.01). When comparing the T-sup-plementatiun group with the controls, there was no statistical difference (P＞0.05). Conclusion: Castration inducedapoptosis in rat corpus cavemosum, that could be prevented by T stupplementat/on, it suggests that androgen plays animportant role in maintaining the structure of corpus cavemusum. (Asian J Androl 1999 Dec; l : 181 - 18S)     

携带ROCK2基因siRNA有效片段的慢病毒载体的筛选

目的:筛选能够显著抑制自发性高血压大鼠(SHR)阴茎海绵体平滑肌细胞内ROCK2基因表达的携带ROCK2基因siRNA的慢病毒载体。方法:设计并合成4个靶向ROCK2的siRNA片段,构建并包装成慢病毒载体。随机将5只SHR阴茎海绵体平滑肌细胞分为6组,每组每个样本3×104个细胞,每组5个样本,分别为:A组(未转染对照组)、B组(携带慢病毒转染组)、C~F组(分别携带靶向ROCK2基因siRNA 1~4号靶点的慢病毒转染组),以感染复(MOI)=80转染SHR阴茎海绵体平滑肌细胞,转染后48 h荧光显微镜下观察细胞GFP表达情况,并用RT-PCR检测各组被转染细胞ROCK2 mRNA的表达。结果:荧光显微镜下观察各组细胞转染效率均50%。与A组相比,B组ROCK2 mRNA的表达无明显改变(P﹥0.05);C、D、F组SHR阴茎海绵体平滑肌细胞ROCK2基因mRNA的表达较A组极显著下降(P0.01),抑制效率分别达到(43.91±8.19)%、(47.15±6.64)%、(25.7±6.03)%;E组SHR阴茎海绵体平滑肌细胞ROCK2基因mRNA的表达较A组显著下降(P0.05),抑制效率为(16.81±5.94)%。结论:本研究构建的4种携带ROCK2基因的siRNA慢病毒载体均能够显著抑制SHR阴茎海绵体平滑肌细胞内ROCK2基因的表达,其中有1种慢病毒载体抑制作用最强。     

Glycated serum albumin decreases connexin 43 phosphorylation in the corpus cavernosum

BackgroundGlycated serum albumin (GSA) is an early glycosylation product that participates in diabetic vascular complications. This study examined the role of GSA in early damage to the corpus cavernosum and the involved mechanisms.MethodsNine 8-week-old male Sprague-Dawley (SD) rats (250–300 g) were divided into the control (saline vehicle, n=3) and GSA (200 µg/kg, n=6) groups. The corpus cavernosum tissues were harvested. Phosphorylated and non-phosphorylated connexin 43 (Cx43), endothelial nitric oxide synthase (eNOS), phosphatidylinositol 3-kinase (PI3K), and serine-threonine kinase (Akt) were tested by immunohistochemistry and western blotting. Human umbilical vein endothelial cells (HUVECs) overexpressing Cx43 were used to analyze the Cx43 phosphorylation sites (S368, S262, Y265, S255, and S279/282) using western blotting.ResultsThe expression of phosphorylated Cx43 in the penis was significantly lower in GSA-treated rats than in controls. The expression levels of p-Cx43, p-eNOS, p-PI3K, and p-Akt were significantly decreased in HUVECs exposed to GSA in dose- and time-dependent manners. The most significant impact on all four proteins was observed with 1 µg/mL of GSA for 12 h. Phosphorylation at the S368, S262, Y265, S255, and S279/282 sites of Cx43 was downregulated by GSA, and S368 was the most significantly suppressed phosphorylation site compared with the other sites.ConclusionsGSA decreases the expression of p-Cx43 in the corpus cavernosum of rats. This effect might be also related to the decreased phosphorylation of p-eNOS, p-PI3K, and p-Akt, as well as by the downregulation of phosphorylation at the S368 site.     

雄激素对大鼠阴茎海绵体平滑肌中兰尼碱受体1和电压门控钙离子通道1.3表达的影响研究

目的:研究兰尼碱受体1(RyR1)和电压门控钙离子通道1.3(CaV1.3)在去势大鼠阴茎海绵体平滑肌的表达,探讨其在去势后勃起功能障碍发生中的作用。方法:40只8周龄雄性SD大鼠随机均分成:假手术2周组(A组),假手术4周组(B组),去势2周组(C组),去势4周组(D组)。术后实验各组检测血清睾酮(T)水平,免疫组化及RT-PCR技术检测RyR1和CaV1.3在大鼠阴茎海绵体平滑肌中的表达。结果:血清T水平C组[(15.97±5.67)nmol/L]和D组[(2.03±1.57)nmol/L]分别较A组[(90.54±20.13)nmol/L]和B组[(120.35±30.32)nmol/L]显著下降(P<0.05)。RyR1、CaV1.3在各组大鼠阴茎海绵体平滑肌中均有表达,RyR1 mRNA相对表达量灰度比值C组(0.51±0.24)和D组(0.33±0.15)分别较A组(1.53±0.25)和B组(1.37±0.23)显著降低(P<0.05);CaV1.3 mRNA相对表达量灰度比值C组(0.50±0.12)和D组(0.32±0.07)分别较A组(1.33±0.05)和B组(1.25±0.03)显著降低(P<0.05)。RyR1蛋白积分光密度值(IA)C组(120.36±25.78)和D组(67.39±30.54)分别较A组(300.96±135.12)和B组(330.38±128.59)显著降低(P<0.05);CaV1.3蛋白IA C组(103.37±39.52)和D组(67.56±20.15)分别较A组(298.68±126.35)和B组(327.35±117.37)显著降低(P<0.05)。雄激素水平与RyR1、CaV1.3在阴茎海绵体平滑肌中的表达水平具有正相关性。结论:雄激素可能通过RyR1、CaV1.3的表达调控阴茎勃起功能。     

淫羊藿苷上调NRF2改善SHR大鼠勃起功能

目的:研究淫羊藿苷是否通过调节核因子类红细胞2-相关因子2(NRF2)通路改善自发性高血压大鼠(SHR)的勃起功能.方法:随机将10周龄健康雄性WKY大鼠(WKR)与雄性SHR大鼠分为4组(每组6只,共24只):WKY对照组、WKR+淫羊藿苷组[10 mg/(kg·d)灌胃]、SHR对照组,SHR+淫羊藿苷组[10 m...     

Testosterone preserves endothelial function through regulation of S1P1/Akt/FOXO3a signalling pathway in the rat corpus cavernosum

The aim of the study was to investigate how testosterone regulating endothelial function in the corpus cavernosum of rats. A total of 32 male Sprague‐Dawley (SD) rats, 10‐weeks‐old, were divided randomly into four groups: normal control group (Control); castration group (Castration); the other 16 rats were castrated followed by testosterone supplementation (orally) every day for 8 weeks: castration +10 mg/kg (lower dose) testosterone group (Castration +LT) and castration +20 mg/kg (high dose) testosterone group (Castration +HT). The data showed that androgen deficiency in the Castration group could induce oxidative stress to attenuate endothelial function, manifested by the impairment of endothelial intercellular junction and endothelial content. This was in parallel with a significant decrease in Akt, Akt target and FOXO3a phosphorylation. Testosterone supplementation in the Castration +LT and Castration +HT groups could greatly preserve testosterone serum levels, endothelial function and erectile function through activation of sphingosine‐1‐phosphate receptor 1 (S1P1)/Akt/FOXO3a pathway. Together, this study suggested that S1P1/Akt/FOXO3a pathway was involved in endothelial dysfunction in the context of androgen deficiency and oxidative stress, which might further explain the mechanism of androgen deficiency inducing ED.     

血红素氧合酶2在慢性肾衰大鼠阴茎海绵体中的表达

目的:检测血红素氧合酶2(HO-2)在慢性肾衰(CRF)大鼠阴茎海绵体中的变化,探讨HO-2在阴茎勃起过程中的作用及与睾酮的关系。方法:采用10周龄雄性SD大鼠行5/6肾切除术构建CRF模型成功后,测定对照组(CTL组,n=15)、CRF组(n=15)平均颈动脉压(MAP)及海绵体内压最大值(ICPmax)、血清睾酮,并检测阴茎海绵体中eNOS、nNOS、HO-2的表达。结果:CRF组在3V、5V电刺激海绵体神经后ICPmax/MAP(0.121±0.084,0.135±0.088)均显著低于对照组(0.263±0.147,0.244±0.089,P<0.01),CRF组血清睾酮浓度[(1.190±0.946)nmol/L]显著低于对照组[(7.800±5.001)nmol/L,P<0.01],CRF组海绵体中nNOS、eNOS表达低于对照组,CRF组海绵体中HO-2表达(0.510±0.397)显著低于对照组(2.672±1.720,P<0.01),海绵体中HO-2表达下降与血清睾酮下降存在相关性(r=0.902,P<0.01)。结论:CRF组大鼠阴茎海绵体中nNOS、eNOS、HO-2、血清睾酮水平降低等可能是CRF并发勃起功能障碍机制之一。     

Aortic eNOS expression and phosphorylation in Apo-E knockout mice: differing effects of rapamycin and simvastatin

BACKGROUND: The inhibition of nitric oxide (NO) by hypercholesterolemia may be mediated, in part, by interactions with caveolin-1 (Cav-1). Because of the facilitatory effects of statins on endothelial function and the adverse effects of rapamycin (RAPA) on plasma lipids, we compared the effects of simvastatin (SMV) and RAPA on endothelial NO synthase (eNOS) and Cav-1 protein expression and phosphorylation in the aortas of apolipoprotein E (Apo-E) knockout (-/-) mice. METHODS: Apo-E -/- mice (n = 38) fed a high-cholesterol diet were given SMV (100 mg/kg/day po), RAPA (3 mg/kg/day ip), or no treatment for 10 weeks. Blood was drawn for serum lipid analysis, and protein was extracted for Western immunoblotting. Selected aortic specimens from 2 animals in each group were examined by histology and immunohistochemistry. The data are expressed as the mean +/- SEM and compared by the Student t test and ANOVA. Significance was established as P < .05. RESULTS: Lipid levels at 10 weeks were similar in the 3 groups except for higher triglyceride levels in RAPA-treated animals. eNOS expression was highest in RAPA-treated mice, but the p-eNOS to eNOS protein expression ratio was significantly greater in the SMV treatment group compared to both RAPA and controls (P < .05). Both Cav-1 and p-Cav-1 expression was significantly lower in the SMV-treated animals (P < .05) compared to mice treated with RAPA. CONCLUSIONS: Although eNOS expression was greatest in the RAPA-treated mice, the expression of p-eNOS was similar in the RAPA- and SMV-treated animals. The increase in eNOS induced by RAPA and the inverse relationship between p-eNOS and Cav-1 protein expression observed with SMV treatment suggest different mechanisms for the regulation of aortic eNOS expression in Apo-E mice by these 2 agents.     

Effects of castration on nitric oxide-mediated relaxations in male rat corpus cavernosum smooth muscle

BACKGROUND: The effects of castration on nitric oxide- mediated relaxations and nitric oxide synthase activity in male rat corpus cavernosum smooth muscles. METHODS: Eight-week-old male rats were assigned to two groups: control (sham operated) and castrated animals. After 8 weeks, corpus cavernosum smooth muscle strips were mounted in an organ bath for isometric tension recordings. Electrical field stimulation (EFS) was applied to the strips precontracted with 30 microM phenylephrine. The microdialysis probe was inserted into the strip, and Krebs-Henseleit solution was perfused into the probe. The dialysate during EFS and cholinergic stimulation was collected, and the amount of NO(-)(2)/NO(-)(3) (NOx) released in the dialysate was measured by the Greiss method. Sodium nitroprusside and carbachol were cumulatively added to the strips precontracted with 30 microM phenylephrine. RESULTS: EFS caused frequency-dependent relaxations and NOx releases in the strips. Pretreatment with N(omega)-nitro-L-arginine (100 microM) and tetrodotoxin (1 microM) completely inhibited relaxations and NOx releases. The maximum relaxation in the castration group was significantly greater than that in the control group. The release of NOx was significantly greater in the castration group than in the control group. Sodium nitroprusside relaxed the tissues in both groups similarly. Carbachol failed either to relax the tissue or to increase the amount of NOx production in the tissue. CONCLUSION: The present data suggest that castration enhances nitric oxide synthase activity and nitric oxide-mediated relaxations in the male rat corpus cavernosum.     

去势对大鼠阴茎海绵体功能和结构的影响

目的 :探讨雄激素对阴茎海绵体功能和结构的影响。　方法 :30只成年雄性大白鼠随机分为 3组 :阉割组、替代组及假手术对照组。于 1周后取阴茎海绵体 ,用紫外分光光度计测定其一氧化氮合酶 (NOS)活性 ,同时用ISEL法检测其细胞凋亡情况。　结果 :阉割组海绵体NOS活性下降 70 %并出现细胞凋亡 (P <0 .0 1) ,睾酮替代能阻止NOS活性降低及凋亡的发生 (P >0 .0 5 )。　结论 :雄激素可通过调节NOS活性及细胞的增殖与凋亡而维持阴茎海绵体的结构与功能。     

Effect of androgen deprivation on penile ultrastructure

Aim: To investigate the ultrastructural changes of penile corpus cavernosum and tunica albuginea in rats treated with castration or finasteride. Methods: Eighteen male Sprague-Dawley rats of nine weeks old were randomly divided into three groups with 6 rats each. Group A served as the control, Group B was castrated and Group C, treated with finasteride. Four weeks later, rats were anesthetized and blood samples obtained for the determination of serum testosterone (T) and dihydrotestosterone (DHT) levels; penile tissues were taken for scanning electron microscopy. Results: The T, free T and DHT levels in Group B and the DHT level in Group C were significantly lower than those in Group A (P<0.05). The tunica albuginea was significantly thinner in Group B than that in Group A (P<0.05), but there was no significant difference between Group C and Group A (P>0.05). Elastic fibers in the tunica albuginea of Group A were very rich and arranged regularly and undulatedly, but in Group B, most of the elastic fibers     

髂内动脉结扎对大鼠阴茎海绵体组织nNOS神经纤维及eNOS表达的影响

目的 研究髂内动脉结扎对大鼠阴茎海绵体组织神经型一氧化氮合酶(nNOS)神经纤维及内皮型一氧化氮合酶(eNOS)表达的影响。方法 45只Wistar雄性成年大鼠随机分为假手术组(21只)和手术组(24只)。其中手术组采用双侧髂内动脉结扎的方法制备动脉性勃起功能障碍(ED)大鼠模型,假手术组作为对照组只切开腹腔不结扎髂内动脉。于术后1周、3周、6周末分别取各组1/3大鼠,观察其勃起功能,并采用免疫组化SP法检测大鼠阴茎组织中nNOS神经纤维的数量及eNOS的表达。结果 手术组与假手术组相比,1周末、3周末和6周末在阴茎勃起次数和阴茎组织nNOS神经纤维数量及eNOS表达上均有显著差异(P<0.01)。手术组大鼠阴茎勃起次数3周末高于1周末,6周末高于3周末;eNOS的表达3周末明显低于1周末,而6周末高于3周末,差异均有显著性意义(P<0.001),并呈增加趋势。手术组大鼠阴茎组织nNOS神经纤维数量三者之间差异均有显著性(P<0.001),呈进行性下降。结论 髂内动脉结扎影响阴茎勃起功能和nNOS、eNOS的表达。阴茎组织中nNOS阳性神经纤维数量的减少,可能是髂内动脉结扎术后阴茎勃起功能障碍发生的原因之一。     

Evidence for the involvement of endothelial nitric oxide synthase from smooth muscle cells in the erectile function of the human corpus cavernosum

Nitric oxide (NO) is an important mediator in the relaxation of cavernosal smooth muscle. The present study examines the existence and location of the constitutive isoform eNOS (endothelial NO synthase) accompanying the already substantiated neurogenic NOS (nNOS) in the human corpus cavernosum of men with and without erectile dysfunction. Activities of NOS enzymes were examined in specimens of 11 potent and nine long-term impotent patients by means of light and electron microscopy using NADPH-diaphorase staining and immunohistochemical eNOS-specific, smooth muscle actin-specific and nNOS-specific markers. Cavernosal smooth muscle shows a distinct expression of eNOS. In contrast to the weaker expression of eNOS and nitrinergic innervation found in larger veins, the small intracavernosal helicine arteries express large quantities of eNOS and possess a dense nitrinergic innervation. Long-term impotent patients display a broad heterogeneity in eNOS expression and nitrinergic innervation while no overall correlation between NOS expression and erectile function was observed. The expression of eNOS indicates eNOS as a main source of NO alongside nNOS. The differentiated localization of eNOS supports at least a role of this isoform in vascular regulation. Received: 21 April 1997 / Accepted 11 November 1997