自发性高血压大鼠阴茎海绵体组织内皮型一氧化氮合酶的表达及意义

目的探讨自发性高血压大鼠(SHR)勃起功能的改变及其发病机制。方法20周龄雄性SHR大鼠及同系正常(WKY)大鼠各10只,夹尾法测量大鼠收缩压(SBP),皮下注射阿朴吗啡(APO)检测阴茎勃起功能,免疫组织化学染色和逆转录-聚合酶链式反应(RT-PCR)法测定海绵体组织内eNOSmRNA的表达。结果SHR组及WKY组收缩压分别为(205.7±11.9)mmHg和(114.3±10.2)mmHg,阴茎勃起次数分别为(0.6±0.5)和(2.4±0.6),差异均具有显著性(P<0.01)。免疫组织化学染色显示eNOS蛋白在WKY大鼠阴茎海绵体组织中普遍表达,在SHR大鼠阴茎海绵体组织内的表达显著低于WKY大鼠(P<0.01)。RT-PCR结果与免疫组化结果相似。结论高血压严重影响阴茎勃起功能,海绵体组织内eNOS的降低可能是自发性高血压大鼠勃起功能下降的机制之一。     

高血压大鼠海绵体平滑肌细胞间连接的变化

目的:比较自发性高血压大鼠(SHR)和正常血压大鼠阴茎海绵体平滑肌细胞间连接改变及与阴茎勃起功能的关系。方法:注射阿朴吗啡(APO)观察14周龄SHR(SHR组,n=5)、W istar-Kyoto大鼠(WKY组,n=5)阴茎勃起情况,用透射电镜观察其阴茎海绵体平滑肌细胞间连接超微结构,RT-PCR测定海绵体平滑肌细胞Connexin 43的mRNA表达,免疫组化观察Connexin 43蛋白表达。结果:SHR组大鼠阴茎勃起次数明显低于WKY组(P<0.05),电镜发现SHR组大鼠阴茎海绵体平滑肌细胞间大量胶原纤维增生,Connexin 43蛋白及其mRNA表达较WKY组显著降低(P<0.05)。结论:高血压影响阴茎勃起功能,阴茎海绵体平滑肌细胞间连接的病理改变可能是高血压性勃起功能障碍的发病机制之一。     

P-Erk1/2和P-Akt1在高血压大鼠阴茎海绵体中的表达

目的:了解磷酸化Erk1/2(P-Erk1/2)和磷酸化Akt1(P-Akt1)在自发性高血压大鼠(SHR)和正常血压大鼠阴茎海绵体中的表达及与勃起功能的关系。方法:健康成年雄性SPF级SHR与对照组WKY大鼠各8只,14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;免疫组织化学及RT-PCR技术检测P-Erk1/2和P-Akt1在大鼠阴茎海绵体的表达。结果:3V和5V电刺激海绵体神经后SHR组ICP/MAP比值(0.26±0.06、0.28±0.04)均较WKY组(0.46±0.12、0.76±0.13)显著降低(P均<0.05),P-Erk1、P-Erk2mRNA和P-Erk1/2蛋白的相对表达量在SHR组(0.81±0.05、0.91±0.06、54.22±10.05)较WKY组(0.42±0.04、0.68±0.14、7.05±1.45)显著升高(P均<0.05);P-Akt1mRNA和P-Akt1蛋白的相对表达量在SHR组(0.90±0.05、11.17±2.21)与WKY组(0.92±0.06、10.91±1.86)无显著差异(P均>0.05)。结论:高血压性勃起功能障碍的发生与阴茎海绵体P-Erk1/2的过度表达有关,而与P-Akt1的表达水平无明显相关。     

自发性高血压大鼠阴茎海绵体组织nNOS变化的实验研究

目的：研究高血压对大鼠阴茎海绵体组织nNOS神经纤维的影响。方法：自发性高血压大鼠(SHR)和同系WKY鼠各12只，都随机分为4周观察组(6只)和12周观察组(6只)。第4周和第12周末时，观察阴茎勃起功能，并检测阴茎组织nNOS神经纤维数目。结果：4周组和12周组中，SHR和WKY鼠在阴茎勃起次数和阴茎组织nNOS神经纤维数目上，都有显著差异(P＜0．01)。SHR4周组和SHR12周组，在阴茎组织nNOS神经纤维数目上，差异也有显著性(P＜0．05)，阴茎勃起次数和勃起率差异无显著性(P＞0．05)，但有减少的趋势。结论：高血压使阴茎组织中nNOS神经纤维数目减少，这可能是高血压引起勃起功能障碍的发病机理之一。     

胱硫醚-γ-裂解酶和胱硫醚-β-合成酶在高血压大鼠阴茎海绵体中的表达

目的:探讨高血压对大鼠阴茎海绵体组织胱硫醚-γ-裂解酶(CSE)和胱硫醚-β-合成酶(CBS)表达的影响及与大鼠勃起功能的关系。方法:健康雄性SPF级自发性高血压大鼠(SHR)与对照组WKY(Wistar-Kyoto)大鼠各10只,于12周龄时测定大鼠血清睾酮、阴茎海绵体内压/平均动脉压(ICP/MAP)、血浆和阴茎海绵体内源性H2S的含量,采用免疫组化和Western印迹分析CSE和CBS在阴茎海绵体内的表达。结果:SHR与WKY大鼠的血清睾酮值没有显著差别,SHR的ICP/MAP在0、3和5 V电刺激盆腔神经节(MPG)时均显著低于WKY组(n=10,P0.05)。SHR血浆H2S含量显著低于WKY大鼠[(10.49±1.35)μmol/Lvs(21.92±2.75)μmol/L,P0.05],SHR阴茎海绵体组织内源性H2S含量显著低于WKY大鼠[(52.60±3.44)nmol/mg prot vs(87.67±2.12)nmol/mg prot,P0.05],SHR阴茎海绵体组织内源性H2S生成率也较WKY大鼠显著降低[(1.14±0.07)nmol/(mg·min)vs(4.35±0.32)nmol/(mg·min),P0.05]。CSE及CBS主要表达在SHR和WKY大鼠阴茎海绵体平滑肌细胞和血管内皮细胞的胞质,SHR的CSE及CBS蛋白表达量均显著低于WKY大鼠(P0.05)。ICP/MAP与CSE和CBS表达呈高度正相关(r=0.955、0.977,P均0.05)。结论:高血压大鼠阴茎海绵体组织中CBS和CSE的表达下降,导致阴茎海绵体内H2S合成减少,可能是高血压引起勃起功能下降的机制之一。     

电刺激阴茎背神经和海绵体内注射药物诱导大鼠阴茎海绵体内压反应

目的:评价阴茎海绵体内压(ICP)监测在电刺激阴茎背神经和海绵体内注射罂粟碱诱导大鼠阴茎勃起反应中的应用。方法:选取性成熟雄性SD大鼠8只,20%氨基甲酸己酯(1000mg/kg)腹腔注射麻醉下,暴露阴茎并解剖阴茎背神经(DN),将充满肝素盐水并连接于压力传感器的25G针头插入一侧海绵体,取另一30G头皮针插入对侧海绵体,分别用于测定ICP和注射血管活性药物。分别以电刺激海绵体神经(刺激参数:电压4V,波幅0.5ms,频率16Hz,持续20s)和海绵体内注射罂粟碱(0.4mg)诱发阴茎勃起,采用SMUPPC型生物信号处理系统记录ICP变化。结果:麻醉大鼠的ICP基线水平为(12.3±3.1)mmHg(1mmHg=0.133kPa),DN电刺激后约30～60sICP明显升高[(36.4±2.3)mmHg,P<0.05],电刺激结束后缓慢下降至基线水平。海绵体内注射罂粟碱后5～8min可诱发ICP明显升高[(28.4±6.1)mmHg,P<0.05]。结论:监测电刺激大鼠DN及海绵体内药物注射诱发的ICP,为阴茎勃起这一复杂神经血管活动的动物模型在体实验研究提供了一种客观准确的科学工具,对于进一步研究阴茎勃起生理和勃起功能障碍的发病机制,评价治疗勃起功能障碍新疗法的疗效等具有重要意义。     

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。     

美蓝抑制侧脑室注射催产素诱发阴茎勃起的实验研究

为阐明阴茎勃起的中枢性机制 ,对 2 0例雄兔进行实验研究显示 :兔基础阴茎海绵体压 (2 .5± 1.8)mmHg ,经侧脑室内注射催产素 5 μg及 10 μg ,可诱发周期性有节律的阴茎海绵体内压升高 ,最高阴茎海绵体平均压分别为 (4 .5± 3.5 )mmHg及 (31± 10 )mmHg。海绵体注射美蓝可抑制催产素的中枢勃起效应 ,间接表明NO仍是阴茎勃起机制中的最重要的神经递质     

人激肽释放酶对离体动物阴茎海绵体平滑肌的舒张效应

目的探讨人组织激肽释放酶对离体动物阴茎海绵体平滑肌的舒张效应,以初步探讨其对阴茎勃起的调节作用。方法通过离体阴茎海绵体平滑肌肌条实验方法,利用PowerLab4SP微弱生物信号采集系统记录人组织激肽释放酶对离体家兔和大鼠阴茎海绵体平滑肌的舒张效应。结果100mU人组织激肽释放酶可分别使去氧肾上腺素诱导的家兔和大鼠阴茎海绵体平滑肌舒张(65.98±6.98)%和(54.86±9.65)%。结论人组织激肽释放酶可强力地舒张离体家兔和大鼠阴茎海绵体平滑肌,推测其对人阴茎海绵体平滑肌也会有较强的舒张效应,可能是勃起功能障碍药物开发的一个新靶点。     

可分泌表达人降钙素基因相关肽重组腺相关病毒对糖尿病大鼠阴茎勃起的作用

目的:探讨重组腺相关病毒(rAAV)介导人降钙素基因相关肽(hCGRP)基因转移在糖尿病大鼠阴茎海绵体平滑肌分泌表达及其对阴茎勃起的作用。方法:建立链佐脲菌素(STZ)糖尿病大鼠模型,随机分为3组,分别将VssHGCMV-hCGRP、VssCMV-GFP和rAAV空病毒液注射于阴茎海绵体。在注射后5 d,采用SMUP-PC型生物信号处理系统检测阴茎背神经电刺激诱发的阴茎勃起反应及海绵体内压(ICP)变化。切取海绵体组织,通过免疫组化技术和激光共聚焦显微镜分别检测hCGRP和绿色荧光蛋白(GFP)表达,以放射免疫法检测组织中环磷酸腺苷(cAMP)和环磷酸鸟苷(cGMP)变化。结果:在VssCMV-GFP转染后5 d,显示阴茎海绵体内几乎所有组织均有广泛的GFP表达,而rAAV空病毒转染的海绵体则无GFP表达。VssHGCMV-hCGRP转染STZ诱导的糖尿病大鼠后5d,电刺激阴茎背神经可诱发明显的阴茎勃起,监测ICP明显增高[(60.5±4.5)mm Hg,1 mm Hg=0.133kPa],而对rAAV空病毒转染的对照组STZ糖尿病大鼠以同样的参数电刺激阴茎背神经则无勃起反应,ICP无明显增加[(22.3±1.3)mm Hg],两组差异有显著性(P<0.01)。免疫组化观察显示在VssHGCMV-hCGRP转染的STZ糖尿病大鼠阴茎海绵体组织中hCGRP表达增强,同时当电刺激阴茎背神经诱发勃起反应时,海绵体内cAMP和cGMP水平均升高,分别为(48.4±6.5)nmol/L和(21.2±13.6)nmol/L,较rAAV空病毒组[(16.7±2.5)nmol/L和(0.42±0.12)nmol/L]明显增高(P<0.01)。结论:经阴茎海绵体内注射重组腺相关病毒VssHGCMV-hCGRP在糖尿病大鼠阴茎海绵体内获得了hCGRP转基因高效表达,其可增加阴茎背神经电刺激诱发的阴茎ICP和勃起反应。     

Candesartan cilexetil protects cavernous tissue in spontaneously hypertensive rats

In previous experiments, our group demonstrated morphological changes in erectile tissue from male spontaneously hypertensive rats (SHR). The present study was performed to determine whether an angiotensin II receptor blocker could protect cavernous tissue (CT) from these structural alterations in SHR. Male SHR and Wistar-Kyoto (WKY) rats were studied during 4 months. Rats were divided into three groups: SHR (n=10), SHR with candesartan cilexetil (n=10) and WKY rats (n=10). Candesartan cilexetil 7.5 mg/kg/day was administered orally throughout the study. CT was processed for pathology studies. The amount of (1) cavernous smooth muscle (CSM), (2) vascular smooth muscle (VSM), (3) collagen type III, and the rat endothelial cell antibody (RECA-1)/tunica media ratio in cavernous arteries were evaluated. SHR with candesartan cilexetil showed a lower blood pressure, a lower percentage of CSM, smaller VSM area, with a higher RECA-1/media ratio, and a lower percentage of collagen type III, when compared to untreated SHR. In addition, SHR showed a positive correlation between systolic blood pressure (SBP) and CSM amount (r=0.91; P<0.01), and SBP and the percentage of collagen type III (r=0.88; P<0.01); these correlations were not observed either in SHR treated with candesartan cilexetil or in WKY rats. We conclude that candesartan cilexetil provides a significant protective role against morphologic changes in vessels as well as in cavernous spaces of the erectile tissue, caused by high blood pressure, in SHR.     

Different effect of losartan and amlodipine on penile structures in male spontaneously hypertensive rats

BACKGROUND: Erectile dysfunction is highly prevalent in hypertensive patients. Since both angiotensin II receptor type-1 blockers (ARBs) and calcium antagonists are current and effective antihypertensive drugs, the aim of this study was to determine possible differences between ARBs and calcium antagonists concerning the protection of penile structures from the deleterious effects of arterial hypertension. METHODS AND RESULTS: During 6 months, 3 groups of male spontaneously hypertensive rats (SHR) and 1 of Wistar-Kyoto (WKY) rats, as a control group, were studied: SHR without treatment; SHR with losartan (L) 30 mg/kg/day; SHR with amlodipine (A) 3 mg/kg/day, and WKY without treatment. Cavernous smooth muscle (CSM) and vascular smooth muscle (VSM) from cavernous arteries, cavernous tissue fibrosis and collagen type III (COL III) were evaluated. After 6 months, SHR+L and SHR+A showed a similar reduction in blood pressure compared with untreated SHR. However, only SHR+L and control WKY presented significantly lower values of: CSM (p < 0.01), VSM (p < 0.01), and COL III (p < 0.01) when compared with either untreated SHR or SHR+A. There was also a positive correlation between left ventricular mass and proteinuria with VSM from cavernous arteries, CSM and COL III in untreated SHR and SHR+A. These relations were not present in SHR+L and WKY. CONCLUSION: Although losartan and amlodipine achieved similar blood pressure control, losartan but not amlodipine showed a significant protective role against structural changes in the vessels and cavernous spaces of the erectile tissue caused by arterial hypertension.     

Ultrastructural comparison of penile cavernous tissue between hypertensive and normotensive rats

Our aim was to compare the ultrastructure of penile cavernous tissue in the spontaneous hypertensive rat (SHR) and normotensive rat, and study the relation of blood pressure with erectile function. After injection of apomorphine (APO), penile erectile frequency in 16-week-old SHR (group A) and Wistar-Kyoto rat (WKY) (group B) was observed and noted. The ultrastructure of the penile cavernous tissue was studied by scanning electron microscope and transmission electron microscope. The mean blood pressures were significantly higher in group A than in group B (P=0; 171.20+/-10.94 and 117.60+/-12.38, n=5, for group A and group B, respectively). After treatment of the two groups with APO, the erectile frequency in group A was significantly less than in group B (P=0.007; 0.40+/-0.55 and 2.40+/-1.14, n=5, for group A and group B, respectively). Significant ultrastructural pathological changes were observed in the tunica albuginea and penile cavernous tissue of SHR. The elastic fibers were decreased and the collagen fibers of the sinusoid were increased in group A. The tunica albuginea thickness (mean+/-s.d.) was 100.20+/-7.22 microm and 126.00+/-7.65 microm in group A and group B, respectively. The tunica albuginea of group A was significantly thinner than that in B (P=0.001). Some endothelial cells and smooth muscle cells exhibited damaged mitochondria, and endoplasmic reticulums and Schwann cells were degenerated in group A. Although the function of penile erection might be affected by a secondary effect related to endothelial dysfunction of hypertension, these ultrastructural pathological changes of the penile cavernous tissue might also be one of the important mechanisms of erectile dysfunction caused by hypertension.     

Morphological modifications in clitoris and vagina in spontaneously hypertensive rats

We evaluated possible morphological alteration in clitoris and vagina from spontaneous hypertensive rats (SHR) and normotensive WKY rats. Clitoris and vagina were processed by Masson's trichrome, anti-alpha-smooth-muscle actin, anticollagen type I (COL I) and type III (COL III), and anti-TGFbeta(1). SHR presented higher amount of clitoral cavernous smooth muscle (CSM), vascular smooth muscle; TGFbeta(1) in clitoral vessel wall; higher wall/lumen ratio in both vaginal and clitoral vessels; and remarkable interstitial fibrosis, expressed by a higher amount in interstitial COL I and III in both clitoris and vagina, compared to WKY rats. Nerve fibers from clitoral and vaginal tissue in SHR showed important fibrosis at perineurium. SHR showed positive correlation between systolic blood pressure (SBP) and clitoral CSM; SBP and fibrosis in clitoris; and SBP and COL I and III in clitoris, respectively. Similar findings were observed between SBP and COL I and III in vagina. In conclusion, SHR present morphologic changes in clitoral vessels as well as in clitoral cavernous space, which have a high positive correlation with the high blood pressure level. Moreover, the increase in extracellular matrix affects not only the clitoral and vaginal interstitium but also the nerve structures from both clitoris and vagina.     

Hypertension superimposed on type II diabetes in Goto Kakizaki rats induces progressive nephropathy

BACKGROUND: Type II diabetes in the Goto Kakizaki (GK) rats (derived from Wistar rats) is not associated with the development of obesity, hyperlipidemia, hypertension, or pronounced renal functional changes. The aim of this study was to investigate the effect of superimposed hypertension on renal function and morphology under conditions of hyper- and normoglycemia. METHODS: The evolution of biochemical and morphologic renal changes was examined in GK and Wistar rats treated with deoxycorticosterone acetate (DOCA) salt over 24 weeks. RESULTS: Blood pressure was increased from 6 weeks on in GK and Wistar rats with no difference in blood pressure levels between both groups (week 24, 183 +/- 14 mm Hg vs. 191 +/- 13 mm Hg, P = NS, vs. 144 +/- 6 mm Hg in normal controls, P < 0.01). A progressive increase in proteinuria was observed in hypertensive GK rats from 12 weeks on (week 24, 168 +/- 62 mg/day vs. 41 +/- 30 mg/day in hypertensive Wistar rats, P = 0.002). Histologic analysis at weeks 15 and 24 showed progressive glomerulosclerosis in hypertensive GK and Wistar rats (week 24, 13 +/- 4% vs. 8 +/- 1%, P = NS) but not in nonhypertensive GK controls. This was associated with evidence of podocyte damage (de novo desmin expression) in hypertensive as compared to nonhypertensive GK rats (week 24, score 1.4 +/- 0.1 vs. 0.8 +/- 0.1, P < 0.001) while no significant increase was observed in hypertensive vs. nonhypertensive Wistar rats. Tubulointerstitial damage was increased in hypertensive GK as compared to hypertensive Wistar rats (week 24, score 1.5 +/- 0.6 vs. 0.6 +/- 0.3, P = 0.01). By immunohistochemistry, this was associated with an up-regulation of tubulointerstitial type IV collagen as well as alpha-smooth muscle actin (alpha-SMA) expression, macrophage infiltration and cell proliferation in hypertensive GK rats. CONCLUSION: Our data demonstrate that long-standing type II diabetes alone is not sufficient to induce progressive nephropathy unless secondary injurious mechanisms such as hypertension are present. The hypertensive GK rat provides a novel model to investigate the mechanisms involved in diabetic nephropathy.     

Effect of N-(biphenylyl-methyl)imidazole, a type 1 angiotensin II receptor inhibitor, on the contractile function of the rat corpus cavernosum

The effect of N-(biphenylyl-methyl)imidazole, losartan potassium, a newly developed antihypertensive type 1 angiotensin II receptor antagonist on the rat erectile function, was studied. Sexually active 9-week-old male spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats were given losartan 60 mg/kg intraperitoneal injections. Mean blood pressure (MBP) dropped significantly in both SHR and WKY rats (for SHR: from 140 +/- 8 to 114 +/- 5 mm Hg, p < 0.05, n = 8; for WKY: from 113 +/- 7 to 79 +/- 9 mm Hg, p < 0.05, n = 8). On the contrary, the intracavernous pressure (ICP) of SHR and WKY rats did not differ significantly from that of the corresponding controls receiving saline injections (p > 0.05, n = 8 for each group). For the chronic study, the rats were fed with losartan 30 mg/kg/day for 30 days. MBP decreased significantly in SHR but not in WKY rats (for SHR: from 137 +/- 7 to 113 +/- 5 mm Hg, p < 0.05, n = 8; for WKY: from 110 +/- 6 to 107 +/- 5 mm Hg, p > 0.05, n = 8). The ICP of the losartan-treated rats was not significantly different from that of control rats (p > 0.05, n = 8 for each group). In contrast, WKY rats receiving guanethidine 1 mg/kg/day for 30 days showed significantly decreased ICP. Angiotensin II (10(-9)-10(-5) M) and losartan (10(-9)- 10(-5) M) did not induce significant contractile responses of the cavernosal strip when tested in vitro. On the other hand, methoxamine 10(-4) M induced good contractile responses. In conclusion, the present study demonstrated that angiotensin II did not cause significant change in the contractile status of rat corpus cavernosum. Correspondingly, the type 1 angiotensin II inhibitor effectively lowered blood pressure but did not affect cavernosal contractile function, thus is useful clinically in the treatment of hypertensive disorders without significant detrimental effects on male sexual function.     

The effect of connective tissue growth factor on renal fibrosis and podocyte injury in hypertensive rats

Objective: The aim of this study was to evaluate the roles of podocalyxin (PCX) and connective tissue growth factor (CTGF) in spontaneously hypertensive rats. Methods: Spontaneously hypertensive rats (SHR) and normotensive control Wistar–Kyoto (WKY) rats were divided into groups referred to as SHR 12W, SHR 24W, WKY 12W and WKY 24W. Systolic blood pressure and 24-hour total uric protein were measured every two weeks in the respective groups. CTGF, PCX, alpha-smooth muscle actin (α-SMA) and collagen-III were evaluated via immunohistochemical staining. In addition, CTGF, PCX, and α-SMA gene expression levels were determined by analyzing mRNA levels. Results: More kidney lesions occurred alongside foot processes effacement in SHR 24W rats than in SHR 12W rats. In SHR 12W rats, blood pressure and 24-hour total uric protein level were elevated and continued to increase thereafter. In the SHR 12W and SHR 24W groups, the expression of CTGF, α-SMA and collagen-III was significantly increased. Immunohistochemical staining showed that PCX expression was significantly reduced in the SHR group and CTGF expression was increased. A significant decrease in PCX mRNA and an increase in CTGF mRNA were observed in SHR 24W rats relative to SHR 12W rats. Conclusion: Both the overexpression of CTGF and the loss of podocalyxin reflect renal damage in spontaneously hypertensive rats. CTGF and PCX may be involved in the mechanisms of podocyte injury and apoptosis induced by hypertension.     

Alterations in nNOS-containing nerve fibers in corpus cavernosum of spontaneous hypertension rats

Objective: To investigate the alterations in nNOS containing nerve fibers in corpus cavernosum of spontaneous hypertension rats (SHR). Methods: Twelve male SHR and 12 male WKY rats, both aged 6 weeks, were separately divided into 4- and 12-week observation groups at random. At the end of the observation period, the erectile function was assessed and the number of cavernosal nNOS containing nerve fibers determined. Results: Significant differences existed in the erection frequency and the number of nNOS containing nerve fibers between the SHR rats and the WKY controls (P< 0.01); there was also a significant difference in the numbers of nNOS containing nerve fibers between the SHR 4- and 12-week observation groups (P<0.05). Conclusion: The erectile function and the number of nNOS containing nerve fibers were significantly reduced in SHR rats. The decrease in nNOS containing nerve fibers may be one of the mechanisms underlying erectile dysfunction in hypertensive rats.     

Influence of hypertension on MAC of halothane in rats

This study was designed to assess the relationship between MAC and hypertension. To this purpose, MAC of halothane was determined in fully inbred spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY). Because MAC determination was performed in animals whose lungs were mechanically ventilated, the adequacy of the ventilation was initially established in 20 rats equally divided into SHR and WKY, and instrumented with catheters in the abdominal aorta. Subsequently, MAC of halothane was determined in 40 rats equally divided into SHR and WKY, including those instrumented. There were no differences in MAC of halothane between SHR (n = 20) and WKY (n = 20) (1.08 +/- 0.02% vs. 1.11 +/- 0.02%). Subgroup analysis indicated that MAC of halothane was not affected by the presence of an arterial catheter in the abdominal aorta (SHR 1.09 +/- 0.06% vs. 1.08 +/- 0.02%; WKY 1.15 +/- 0.04% vs. 1.08 +/- 0.02%). The authors' data provide experimental evidence that MAC is not affected by either chronic hypertension or limited instrumentation.