侧脑室注射血管紧张素Ⅱ对大鼠血压和缰核内神经元电活动的影响

实验观察了侧脑室注射（ｉｃｖ）及缰核（ｈａｂｅｎｕｌａ ｎｕｃｌｅｕｓ）内微电泳血管紧张素Ⅱ（ＡⅡ）与「Ｓａｒ＾１,Ｔｈｒ＾３」－ＡⅡ（ＳＴ－ＡⅡ,ＡⅡ拮抗剂）对正常和诮激性高血压（ｓｔｒｅｓｓ－ｉｎｄｕｃｅｄ ｈｙｐｅｒｔｅｎｓｉｏｎ ＳＩＨ）大鼠血压及内外侧缰核（ＭＨｂ、ＬＨｂ）内心血管神经元入电活动的影响。结果如下：ｉｃｖ ＡⅡ或ＳＴ－ＡⅡ,正常鼠和ＳＩＨ大鼠血压均升高或降低,ＳＩＨ鼠较正常     

损毁缰对应激性高血压形成的影响

目的和方法：运用核团损毁和微量注射的方法观察损毁缰核（Ｈｂ）对应激性高血压（ＳＩＨ）形成进程的影响及ＳＩＨ大鼠Ｈｂ内神经元对Ｌ－谷氨酸反应性的变化。结果：（１）损毁双侧Ｈｂ延缓了ＳＩＨ的形成进程;（２）在ＳＩＨ大鼠内侧Ｈｂ（ＭＨｂ）微量注射不同浓度的ＣＩｕ,血压明显升高;呈浓度依赖性,升高值与正常大鼠ＭＨｂ注入等量Ｇｌｕ引起的升高值相比,有显著性差异;（３）在ＳＩＨ大鼠外侧Ｈｂ（ＬＨｂ）注入不同浓     

大鼠最后区内微量注射血管紧张素Ⅱ对肾脏排钠的影响

已知最后区存在血管紧张素ⅡＡ（Ⅱ）受体,并可感受血中ＡⅡ水平的变化,本文采用微量注射ＡⅡ于ＡＰ的方法,观察了ＡＰ和肾功能的关系。结果：ＡＰ内微量注射ＡⅡ（２．２０ｎｇ）引起肾小球滤过率（ＧＦＲ）,肾血浆流量（ＲＰＦ）,尿钠排泄（ＵＮａＶ）的增加（Ｐ〈０．０５）。该作用可被ＡＰ内微量注射ＡⅡ拮抗剂ｓａｒａｌａｓｉｎ或切断（Ｐ〈０．０５）。而静脉注射ｓａｒａｌａｓｉｎ却不能阻断该作用。微量注射ＡⅡ于弧     

蛋白激酶C在血管紧张素Ⅱ抑制心肌细胞——氧化氮合成中的作用

实验用硝酸还原酶法测定培养新生大鼠内肌细胞亚硝酸盐（ＮＯ２）和硝酸盐（ＮＯ３）总量（ＮＯ２／ＮＯ３）,反映心肌细胞一氧化氮（ＮＯ）生成情况,观察血管紧张素Ⅱ（ＡｎｇⅡ）对凡肌细胞ＮＯ生成的及其蛋白激酶Ｃ（ＰＫＣ）在该效应中的作用。结果显示：ＡｎｇⅡ可减少心肌细胞ＮＯ的含量,并具有明显的剂量－效应关系;ＡｎｇⅡ受体拮抗剂ｓａｒａｌａｓｉｎ可明显抵制ＡｎｇⅡ对ＮＯ生成的影响;Ｌ－精氨酸（Ｌ－Ａｒｇ）明     

血管紧张素Ⅱ诱导培养的成年大鼠心肌细胞凋亡及其细胞机制

研究血管紧张素Ⅱ（ＡｎｇｉｏｔｅｎｓｉｎⅡ,ＡｎｇⅡ）诱导培养的成年大鼠心肌细胞（Ａｄｕｌｔｒａｔｖｅｎｔｒｉｃｕｌａｒｍｙ－ｏｃｙｔｅｓ,ＡＲＶＭ）凋亡。酶灌流消化法分离培养ＡＲＶＭ,不同处理后,光镜观察形态改变,琼脂糖凝胶电泳定性分析ＤＮＡ降解程度。结果发现培养的ＡＲＶＭ经１０μｍｏｌ／ＬＡｎｇⅡ处理４８ｈ后,大部分细胞变圆,胞浆浓缩;电泳显示核酸断裂片段“梯形”结构,上述改变在７２ｈ更为明显。上述作用可被氯沙坦、维拉帕米和ｓｔａｕｒｏｓｐｏｒｉｎｅ所取消。结果表明,ＡｎｇⅡ诱导培养的ＡＲＶＭ凋亡由ＡＴ１受体介导、细胞内钙升高和ＰＫＣ激活起重要作用     

运动对高血压性肥大心脏心肌肌球蛋白重链基因表达的影响

研究运动逆转高血压肥大心脏心肌肌球蛋白重链（ｍｙｏｓｉｎ ｈｅａｖｙ ｃｈａｉｎ ,ＭＨＣ）异型改变的分子机制。方法：采用Ｎｏｒｔｈｅｒｎ 分子杂交方法对自发性高血压大鼠（ｓｐｏｎｔａｎｅｏｕｓｌｙ ｈｙｐｅｒｔｅｎｓｉｖｅ ｒａｔｓ,ＳＨＲ） 游泳运动１０ 周后心肌ＭＨＣ基因表达进行比较研究。结果：游泳ＳＨＲ收缩压和舒张压分别比安静ＳＨＲ 降低２２ ％ 和２５％ （Ｐ＜ ０．０１） 。左心室重／体重（ＬＶＷ／ＢＷ）比值两组间无明显差异（Ｐ＞ ０．０５）。游泳ＳＨＲ 心肌αＭＨＣｍＲＮＡ表达比安静ＳＨＲ增强１７％ ,βＭＨＣｍＲＮＡ 表达降低２６ ％ ,α／βＭＨＣ基因表达比值提高５９ ％ 。结论：运动逆转高血压肥大心脏心肌ＭＨＣ同型异构体转变的调控机制可发生在基因转录水平上     

低氧、血管紧张素Ⅱ对肺内小动脉平滑肌细胞膜Ca2 ┐ATPase活力的影响

本课题观察了低氧及血管紧张素Ⅱ（ａｎｇｉｏｔｅｎｓｉｎⅡ,ＡｎｇⅡ）对分离培养家兔肺内小动脉平滑肌细胞（ＰＡＳＭ－Ｃｓ）膜Ｃａ２＋－ＡＴＰａｓｅ活力的影响,同时用钙通道阻断剂维拉帕米（ｖｅｒａｐａｍｉｌ,ＶＰ）进行干预,进一步了解细胞内钙与Ｃａ２＋－ＡＴＰａｓｅ活力的关系。结果表明：ＰＡＳＭＣｓ膜Ｃａ２＋－ＡＴＰａｓｅ活力对低氧具有短暂的耐受性,随低氧时间延长,Ｃａ２＋－ＡＴＰａｓｅ活力呈时间依赖性抑制;低氧、ＡＮＧⅡ均能抑制Ｃａ２＋－ＡＴＰａｓｅ活力（Ｐ＜０．０１）低氧＋ＡⅡ对Ｃａ２＋－ＡＴＰａｓｅ活力的抑制具叠加效应（Ｐ＜０．０５）;ＶＰ可逆转低氧、ＡｎｇⅡ、低氧＋ＡｎｇⅡ对Ｃａ２＋－ＡＴＰａｓｅ活力的抑制（Ｐ＜０．０１）。结果提示：低氧,ＡＮＧⅡ可通过抑制肺血管平滑肌细胞膜Ｃａ２＋－ＡＴＰａｓｅ活力而可能削弱肺血管平滑肌舒张功能也可能是低氧性肺动脉高压（ＨＰＨ）形成的原因之一。     

pp60c-src在血管平滑肌细胞内丝裂原活化蛋白激酶激活中的作用

观察ｐｐ６０ｃ－ｓｒｃ在血管紧张素Ⅱ（ＡｎｇⅡ）诱导血管平滑肌细胞（ＶＳＭＣｓ）内丝裂原活化蛋白激酶（ＭＡＰＫ）激活中的作用,以了解ＡｎｇⅡ促ＶＳＭＣｓ增殖的信号转导过程。将合成的反义ｃ－ｓｒｃ寡脱氧核苷酸（ｏｌｉｇｏｄｅｏｘｙｎｕｃｌｅ－ｏｔｉｄｅｓ,ＯＤＮｓ）以脂质体包裹转染培养的大鼠ＶＳＭＣｓ,用Ｗｅｓｔｅｒｎ印迹测得细胞裂解液中ｐｐ６０ｃ－ｓｒｃ含量明显下降,免疫沉淀方法测得ｐｐ６０ｃ－ｓ     

心脏肾素－血管紧张素系统在游泳引起的生理性心肌肥大中的作用

本实验采用游泳训练（ＳＷ）引起的大鼠心肌肥大模型,通过放射免疫及生化等方法,对生理性心肌肥大时,心脏和循环肾素－血管紧张素系统（ＲＡＳ）的变化进行了初步研究。观察到游泳五周时,大鼠左、右心室重与体重比值（Ｖ／Ｂｗｔ）显著升高,同时,左、右室心肌血管紧张素Ⅱ（ＡｎｇⅡ）含量及心肌Ａｎｇ转换酶（ＡＣＥ）活性也较对照组明显升高（Ｐ＜０．０５）。心肌ＡｎｇⅡ与Ｖ／Ｂｗｔ之间存在明显的正相关关系（ｒ＝０．７７２１,Ｐ＜０．００１）。ＳＷ组血浆ＡｎｇⅠ,Ⅱ及肾素活性（ＲＡ）与对照组相比无明显差异,其血浆ＡｎｇⅡ与Ｖ／Ｂｗｔ之间无明显相关性。上述研究提示：心脏ＲＡＳ在ＳＷ引起的生理性心肌肥大中可能起着重要作用,而且这种作用在很大程度上不依赖于循环ＲＡＳ。     

肾神经传入纤维在DOCA─salt大鼠高血压形成中的作用

于大鼠皮下埋入含醋酸去氧皮质酮（ＤＯＣＡ）的硅胶管以形成ＤＯＣＡ－ｓａｌｔ高血压,其中一组动物在埋管前切除（Ｔ＿９－Ｌ＿２）脊髓右侧背根神经,每周以尾套法测定大鼠收缩压,埋管后６周测定大鼠脑和血浆中儿茶酚胺（ＣＡ）和血管紧张素Ⅱ（ＡｎｇⅡ）的浓度,用电脑血管显微图像分析系统测量血管的结构变化。与对照鼠相比,ＤＯＣＡ－ｓａｌｔ高血压大鼠下丘脑和延脑的肾上腺素含量和ＡｎｇⅡ放免活性及血浆去甲肾上腺素（ＮＥ）浓度均明显增加,血浆ＡｎｇⅡ浓度降低,心系数（心重／体重）和肠系膜动脉的中层厚度、壁厚与腔径（壁腔）比值增大;切除脊髓背根可明显延缓ＤＯＣＡ－ｓａｌｔ高血压的形成、预防以上组织ＣＡ浓度和ＡｎｇⅡ放免活性增加以及缓解心肌和血管平滑肌的肥厚。提示,肾神经传入纤维在ＤＯＣＡ－ｓａｌｔ高血压形成中起作用,其机制可能通过影响脑内肾上腺素能神经元和激活脑肾素－血管紧张素系统增加交感传出而起作用。     

The Effects of Angiotensin II and Angiotensin-(1–7) in the Rostral Ventrolateral Medulla of Rats on Stress-Induced Hypertension

We have shown that angiotensin II (Ang II) and angiotensin-(1–7) [Ang-(1–7)] increased arterial blood pressure (BP) via glutamate release when microinjected into the rostral ventrolateral medulla (RVLM) in normotensive rats (control). In the present study, we tested the hypothesis that Ang II and Ang-(1–7) in the RVLM are differentially activated in stress-induced hypertension (SIH) by comparing the effects of microinjection of Ang II, Ang-(1–7), and their receptor antagonists on BP and amino acid release in SIH and control rats. We found that Ang II had greater pressor effect, and more excitatory (glutamate) and less inhibitory (taurine and γ-aminobutyric acid) amino acid release in SIH than in control animals. Losartan, a selective AT₁ receptor (AT₁R) antagonist, decreased mean BP in SIH but not in control rats. PD123319, a selective AT₂ receptor (AT₂R) antagonist, increased mean BP in control but not in SIH rats. However, Ang-(1–7) and its selective Mas receptor antagonist Ang779 evoked similar effects on BP and amino acid release in both SIH and control rats. Furthermore, we found that in the RVLM, AT₁R, ACE protein expression (western blot) and ACE mRNA (real-time PCR) were significantly higher, whereas AT₂R protein, ACE2 mRNA and protein expression were significantly lower in SIH than in control rats. Mas receptor expression was similar in the two groups. The results support our hypothesis and demonstrate that upregulation of Ang II by AT₁R, not Ang-(1–7), system in the RVLM causes hypertension in SIH rats by increasing excitatory and suppressing inhibitory amino acid release.     

The levels of renin-angiotensin related components are modified in the hippocampus of rats submitted to pilocarpine model of epilepsy

We previously showed that patients with temporal lobe epilepsy (TLE) present an increased expression of angiotensin II (AngII) AT1 and AT2 receptors in the hippocampus, supporting the idea of an upregulation of renin-angiotensin system (RAS) in this disease. This study aimed to verify the relationship between the RAS and TLE during epileptogenesis. Levels of the peptides angiotensin I (AngI), angiotensin II (AngII) and angiotensin 1-7 (Ang 1-7), were detected by HPLC assay. Angiotensin AT1 and AT2 receptors, Mas mRNA receptors and angiotensin converting enzyme (ACE), tonin and neutral endopeptidase (NEP) mRNA were also quantified at the hippocampus of Wistar rats by real time PCR, during acute (n=10), silent (n=10) and chronic (n=10) phases of pilocarpine-induced epilepsy. We observed an increased peptide level of Ang1-7 into acute and silent phases, decreasing importantly (p≤0.05) in the chronic phase, suggesting that AngI may be converted into Ang 1-7 by NEP, which is present in high levels in these periods. Our results also showed increased peptide level of AngII in the chronic phase of this model. In contraposition, the ACE expression is reduced in all periods. These data suggest that angiotensinogen or AngI may be cleaved to AngII by tonin, which showed increased expression in all phases. We found changes in AT1, AT2 and Mas mRNA receptors levels suggesting that Ang1-7 could act at Mas receptor during the silent period. Herein, we demonstrated for the first time, changes in angiotensin-related peptides, their receptors as well as the releasing enzymes in the hippocampus of rats during pilocarpine-induced epilepsy.     

Altered cardiovascular responses to chronic angiotensin II infusion in aged rats

In this work we determined by telemetry the cardiovascular effects produced by Ang II infusion on blood pressure (BP) and heart rate (HR) in aged rats. Male Wistar aged (48-52 weeks) and young (12 weeks) rats were used. Ang II (6 microg/h, young, n=6; aged, n=6) or vehicle (0.9% NaCl 1 microl/h, young, n=4; aged, n=5) were infused subcutaneously for 7 days, using osmotic mini-pump. The basal diurnal and nocturnal BP values were higher in aged rats (day: 98+/-0.3 mm Hg, night: 104+/-0.4 mm Hg) than in the young rats (day: 92+/-0.2 mm Hg, night: 99+/-0.2 mm Hg). In contrast, the basal diurnal and nocturnal HR values were significantly smaller in the aged rats. Ang II infusion produced a greater increase in the diurnal BP in the aged rats (Delta MAP=37+/-1.8 mm Hg) compared to the young ones (Delta MAP=30+/-3.5 mm Hg). In contrast, the nocturnal MAP increase was similar in both groups (young rats; Delta MAP=22+/-3.0 mm Hg, aged rats; Delta MAP=24+/-2.6 mm Hg). During Ang II infusion HR decreased transiently in the young rats. An opposite trend was observed in the aged rats. Ang II infusion also inverted the BP circadian rhythm, in both groups. No changes in HR circadian rhythm were observed. These differences suggest that the aging process alters in a different way Ang II-sensitive neural pathways involved in the control of autonomic activity.     

Evidence for a role of AT(2) receptors at the CVLM in the cardiovascular changes induced by low-intensity physical activity in renovascular hypertensive rats

In the present study, we evaluated the involvement of the rennin-angiotensin system (RAS) in the control of the blood pressure (BP), baroreceptor-mediated bradycardia and the reactivity of caudal ventrolateral medulla (CVLM) neurons to Ang II and to AT(2) receptor antagonist in sedentary or trained renovascular hypertensive rats. Physical activity did not significantly change the baseline mean arterial pressure (MAP), heart rate (HR) or the sensitivity of the baroreflex bradycardia in normotensive Sham rats. However, in 2K1C hypertensive rats, physical activity induced a significant fall in baseline MAP and HR and produced an improvement of the baroreflex function (bradycardic component). The microinjections of Ang II into the CVLM produced similar decreases in MAP in all groups, Sham and 2K1C, sedentary and trained rats. The hypotensive effect of Ang II at the CVLM was blocked by previous microinjection of the AT(2) receptors antagonist, PD123319, in all groups of rats. Unexpectedly, microinjection of PD123319 at the CVLM produced a depressor effect in 2K1C sedentary that was attenuated in 2K1C trained rats. No significant changes in MAP were observed after PD123319 in Sham rats, sedentary or trained. These data showed that low-intensity physical activity is effective in lowering blood pressure and restoring the sensitivity of the baroreflex bradycardia, however these cardiovascular effects are not accompanied by changes in the responsiveness to Ang II at CVLM in normotensive or hypertensive, 2K1C rats. In addition, the blood pressure changes observed after AT(2) blockade in 2K1C rats suggest that hypertension may trigger an imbalance of AT(1)/AT(2) receptors at the CVLM that may be restored, at least in part, by low-intensity physical activity.     

Angiotensin II and 1-7 during aging in Metabolic Syndrome rats. Expression of AT1, AT2 and Mas receptors in abdominal white adipose tissue

Renin-Angiotensin System (RAS) plays an important role in the development of Metabolic Syndrome (MS) and in aging. Angiotensin 1-7 (Ang 1-7) has opposite effects to Ang II. All of the components of RAS are expressed locally in adipose tissue and there is over-activation of adipose RAS in obesity and hypertension. We determined serum and abdominal adipose tissue Ang II and Ang 1-7 in control and MS rats during aging and the expression of AT1, AT2 and Mas in white adipose tissue. MS was induced by sucrose ingestion during 6, 12 and 18 months. During aging, an increase in body weight, abdominal fat and dyslipidemia were found but increases in aging MS rats were higher. Control and MS concentrations of serum Ang II from 6-month old rats were similar. Aging did not modify Ang II seric concentration in control rats but decreased it in MS rats. Ang II levels increased in WAT from both groups of rats. Serum and adipose tissue Ang 1-7 increased during aging in MS rats. Western blot analysis revealed that AT1 expression increased in the control group during aging while AT2 and Mas remained unchanged. In MS rats, AT1 and AT2 expression decreased significantly in aged rats. The high concentration of Ang 1-7 and adiponectin in old MS rats might be associated to an increased expression of PPAR-γ. PPAR-γ was increased in adipose tissue from MS rats. It decreased with aging in control rats and showed no changes during aging in MS rats. Ang 1-7/Mas axis was the predominant pathway in WAT from old MS animals and could represent a potential target for therapeutical strategies in the treatment of MS during aging.     

Angiotensinase and vasopressinase activities in hypothalamus, plasma, and kidney after inhibition of angiotensin-converting enzyme: basis for a new working hypothesis

Reducing angiotensin II (Ang II) production via angiotensin-converting enzyme (ACE) inhibitors is a key approach for the treatment of hypertension. However, these inhibitors may also affect other enzymes, such as angiotensinases and vasopressinase, responsible for the metabolism of other peptides also involved in blood pressure control, such as Ang 2-10, Ang III, Ang IV, and vasopressin. We analyzed the activity of these enzymes in the hypothalamus, plasma, and kidney of normotensive adult male rats after inhibition of ACE with captopril. Aspartyl- (AspAP), glutamyl- (GluAP), alanyl- (AlaAP) and cystinyl-aminopeptidase (CysAP) activities were measured fluorimetrically using arylamides as substrates. Systolic blood pressure (SBP), water intake, and urine flow were also measured. Captopril reduced SBP and increased urine flow. In the hypothalamus, GluAP and AspAP increased, without significant changes in either AlaAP or CysAP. In contrast with effects in plasma, GluAP was unaffected, AspAP decreased, while AlaAP and CysAP increased. In the kidney, enzymatic activities did not change in the cortex, but decreased in the medulla. These data suggest that after ACE inhibition, the metabolism of Ang I in hypothalamus may lead mainly to Ang 2-10 formation. In plasma, the results suggest an increased formation of Ang IV together with increased vasopressinase activity. In the kidney, there is a reduction of vasopressinase activity in the medulla, suggesting a functional reduction of vasopressin in this location. The present data suggest the existence of alternative pathways in addition to ACE inhibition that might be involved in reducing BP after captopril treatment.     

孕烷醇酮对应激性高血压大鼠血压的影响

实验探讨了孕烷醇酮(pregnanolone,PGN)对应激性高血压(stress-induced hypertension,SIH)大鼠血压影响的可能机制。采用电击足底结合噪声应激刺激的方法制备应激性高血压大鼠模型,观察每天应激刺激前腹腔注射PGN(0.24 mg/kg)对应激大鼠血压的影响,并观察PGN对应激刺激引起大鼠血中血管紧张素Ⅱ(angiotensin Ⅱ,Ang Ⅱ)含量和大鼠脑内Fos蛋白样免疫反应(FLI)神经元表达的影响。将动物随机分为正常对照组、应激1 h组、应激1 h PGN组、应激15 d组和应激15 d PGN组。实验结果如下:应激15 d PGN组大鼠尾动脉收缩压升高幅值较应激15 d组大鼠尾动脉收缩压升高幅值明显降低(P<0.001)。同时,应激1 h组及应激15 d组血中Ang Ⅱ含量与对照组相比有显著升高(均P<0.001);应激1 h PGN组及应激15 d PGN组大鼠血中Ang Ⅱ含量分别显著低于应激1 h组及应激15 d组(均P<0.05);应激15 d组血中Ang Ⅱ含量较应激1 h组高(P<0.05)。正常对照组、应激15 d组、应激15 d PGN组大鼠脑内仅见少数FLI神经元。与对照组相比,应激1 h组大鼠脑内外侧缰核(LHb)、内侧缰核(MHb)、室旁核(PVN)、杏仁中央核(CeA)和下丘脑外侧区(LH)等部位可见FLI神经元显著增加,而腹腔注射PGN后再应激1 h,可抑制上述效应。结果提示,PGN可抑制SIH大鼠血压升高的程     

Angiotensin in the brain suppresses epinephrine-induced cardiac arrhythmias through CNS opioid mechanisms.

To test the hypothesis that angiotensin II (Ang II) in the central nervous system modulates catecholamine-induced cardiac arrhythmias and to determine whether endogenous opioids are operative in this action, arrhythmias were produced in male Wistar rats, by continuous infusion of epinephrine at incremental doses until the development of fatal arrhythmias that were usually ventricular fibrillation. Rats were instrumented with catheters in the lateral cerebral ventricle, femoral vein and femoral artery. Ang II, 0.5 microgram, in the lateral cerebral ventricle (ICV) markedly and significantly (p less than 0.05) increased the epinephrine dose, at the occurrence of ventricular premature beats compared to the control group 228 +/- 11 (SEM) vs 116 +/- 7 micrograms epinephrine/kg and at the onset of fatal arrhythmias 225 +/- 13 vs 185 +/- 9 micrograms epinephrine/kg. Ang II, 0.5 microgram i.v., did not affect arrhythmia threshold. The angiotensin converting enzyme inhibitor captopril, 1 mg/kg, decreased arrhythmia threshold as ventricular arrhythmias were first noted at 106 +/- 4 and fatal arrhythmias occurred at 118 +/- 4 micrograms epinephrine/kg. The Ang II receptor antagonist saralasin 150 micrograms/kg ICV, blunted and 300 micrograms/kg ICV reversed the effect of Ang II. The mu opioids antagonist naloxone and the kappa opioid antagonist MR 2266, 50 micrograms/kg ICV, prevented the effect of Ang II on fatal arrhythmias. The action Ang II on arrhythmias could not be explained by the effects of Ang II on blood pressure or heart rate. These data indicate a role for Ang II within the CNS to modulate cardiac arrhythmias and that this is mediated in part, by endogenous opioids.     

Effect of angiotensin II and saralasin on motor activity and the passive avoidance behavior of rats

One nmole of angiotensin II (ANG II) or saralasin, given intracerebroventricularly, failed to alter the motor activity of rats in open field. A combined injection of both peptides caused a significant decrease of the number of crossings and rearings. In the electromagnetic motimeter horizontal activity of animals was changed by neither of the peptides while the vertical activity was increased by ANG II. Again, a combined injection of saralasin and ANG II inhibited both horizontal and vertical activity. Stereotypies evoked by both apomorphine (2 mg/kg) and amphetamine (6.5 mg/kg), given intraperitoneally, were markedly intensified by ANG II and saralasin. A five-fold increase of the re-entry latencies in the passive avoidance situation was observed after pre-test administration of ANG II or saralasin but not the two in combination. These results suggest that ANG II and saralasin may improve processes related to learning and memory through an unspecific mechanism involving central dopamine systems.