植物雌激素白藜芦醇和根皮素对家兔离体主动脉收缩反应的影响(英文)

目的探讨植物雌激素白藜芦醇和根皮素对离体主动脉血管收缩的舒张作用特点是否同雌激素以及有关的作用机制。方法将家兔离体主动脉平滑肌条置于灌流肌槽中,记录其等长张力变化。结果白藜芦醇和根皮素可明显抑制离体血管对去甲肾上腺素(NE)、KCl和CaCl2的浓度依赖性收缩反应,使其量效曲线明显右移, pD2′值分别为2.89,3.34, 3.37和3.23, 3.52, 3.77;对KCl预收缩血管条具有浓度依赖性的舒张效应。去除血管内皮、Nω-L-硝基精氨酸(L-NNA)或亚甲蓝对白藜芦醇舒张血管作用具有明显的抑制作用,但对根皮素诱发的血管舒张无明显影响。吲哚美辛和普萘洛尔温育后,对二者的舒血管作用均无明显影响。在无钙Krebs液(含0.01 mmol·L-1EGTA)中,白藜芦醇和根皮素可抑制NE诱发的由肌细胞内钙释放引起的Ⅰ相收缩,但不影响CaCl2诱发的由肌细胞外钙内流引起的Ⅱ相收缩。结论白藜芦醇和根皮素对离体主动脉血管的舒张作用可能与其抑制钙离子内流及细胞内钙释放有关;另外白藜芦醇的舒张作用部分与内皮细胞有关,但根皮素的舒血管作用与内皮细胞无关。     

阿司匹林铜对离体兔主动脉血管条收缩的影响(英文)

目的:观察阿司匹林铜对离体免胸主动脉血管平滑肌的作用。方法:取免胸主动脉条,观察阿司匹林铜对去甲肾上腺素(NE)、KCl、CaCl_2诱导收缩作用的影响。结果:证实阿司匹林铜和对照物硫酸铜拮抗NE诱导的兔胸主动脉条收缩,IC_(50)分别为31nmol/L和0.29μmol/L,而阿司匹林本身没有拮抗作用。阿司匹林铜对KCl、CaCl_2诱导的收缩没有影响。在去内皮细胞兔胸主动脉条上,观察到相同的作用。结论:阿司匹林铜具有较强的拮抗NE诱导离体兔胸主动脉条收缩的作用,但不能拮抗KCl、CaCl_2诱导的收缩,提示阿司匹林铜通过阻断受体调控钙通道,舒张血管平滑肌。     

高浓度葡萄糖抑制兔胸主动脉内皮依赖的血管舒张(英文)

目的:研究高浓度葡萄糖是否能抑制兔胸主动脉内皮依赖的血管舒张以及可能的机制。方法:利用器官组织浴动脉环法测定血管张力,观察去除内皮、NO合酶抑制剂L-NMMA,不同浓度的葡萄糖对乙酰胆碱(ACh)产生的内皮依赖的和硝普钠(SNP)产生的非内皮依赖的血管舒张功能的影响以及维生素C和膜渗透性抗氧化剂MnTMPyP对高浓度葡萄糖作用的影响。结果:ACh和SNP均产生浓度依赖的血管舒张效应,高浓度葡萄糖明显抑制ACh产生的血管舒张,而对SNP的作用无明显影响,维生素C和MnTMPyP不能逆转高浓度葡萄糖对ACh产生的血管舒张的抑制作用。结论:高浓度葡萄糖抑制内皮依赖的血管舒张,这种作用不是通过增加氧自由基的产生介导的。     

Relaxation effects of matrine on guinea-pig aortic smooth muscles

Objective The present in vivo study was undertaken to determine whether matrine,a kind of traditional Chinese medicinal alkaloid,would relax the isolated guinea pig aortic smooth muscles,if so,to investigate the mechanism involved.Methods The concentration-dependent relaxation response to matrine was studied in phenylephrine or potassium chloride precontracted guinea pig aortic rings.Results Matrine(1×10-4 M-3.3×10-3 M)relaxed the endothelium denuded aortic rings precontracted submaximally with phenylephrine,in a concentration-dependent manner,and it's preincubation(3.3×10-3 M)produced a significant rightward shift in the phenylephrine dose-response curve,but had no effects on the potassium chloride-induced contraction.The anticontractile effect of matrine was not reduced by the highly selective ATP-dependent K+ channel blocker glibenclamide(10-5 M),the non-selective K+ channel blocker tetraethylammonium(10-3 M),as well as the β-antagonist propranolol(10-5 M).In either "normal" or "Ca2+-free" bathing medium,the phenylephrine-induced contraction was attenuated by matrine(3.3×10-3 M),indicating the vasorelaxation was due to inhibit of intracellular and extracellular Ca2+ mobilization.Conclusions The results obtained clearly demonstrated that matrine inhibits phenylephrine-induced contractions by inhibiting activation of α-adrenoceptor and interfering with both the release of intracellular Ca2+ and the influx of extracellular Ca2+.     

Effects of Panax notoginseng saponins on vascular endothelial cells in vitro

AIM: To investigate the inhibition of endothelium-de-pendent in vitro vascular relaxation induced by the total saponins (gensenosides) from Panax notoginseng (PNS) and the effect of PNS on the cytosolic Ca2 concentration on cultured bovine pulmonary artery endothelial cells. METHODS: The endothelial-dependent vascular relaxation was assessed using acetylcholine (ACh) or cyclopi-azonic acid (CPA) induced relaxation in endothelium-intact rat aorta. Cytosolic Ca2 level was assessed in real time using dynamic digital fluorescence ratio imaging. RESULTS: In addition to its direct relaxation of the smooth muscle cells at high concentrations, PNS, at 100 mg/L having little effect on smooth muscle, caused a marked inhibition of endothelium-dependent relaxation brought about by PNS. This inhibitory effect was due to its inhibition of elevation of cytosolic Ca2 , which is required for the activation of NO generation and release from the vascular endothelial cells. Nifedipine has no effect on either the endothe     

Evidence for a common defect associated with pressure in the aorta of two hypertensive rat strains

1. Thoracic aortas of normotensive (Wistar-Kyoto (WKY) and Lyon normotensive (LN)) and hypertensive (spontaneously hypertensive rats (SHR) and Lyon hypertensive (LH)) rats from two groups (Japanese (WKY rats and SHR) and Lyon (LN and LH rats)) were compared using organ chambers. Changes in endothelium and smooth muscle reactivity to noradrenaline (NA), carbamylcholine and N omega-nitro-L-arginine (L-NNA) were analysed to distinguish between changes in reactivity that are associated with the presence of hypertension and those that are dependent on group (Japanese vs Lyon). 2. Aortas of hypertensive rats had lower pD2 values for NA than aortas from normotensive rats. These differences were associated with hypertension (P < 0.005 and P < 0.01) and group (P < 0.005 and P < 0.005) in presence or absence of endothelium, respectively, whereas no difference was seen in the maximal developed tension in response to NA. 3. Aortas also differed by a reduced ability to relax in response to carbamylcholine in hypertensive rats; this effect is hypertension (P < 0.05) and group (P < 0.005) dependent, without any change in carbamylcholine pD2 values. 4. Changes in maximum developed tension in the presence of L-NNA were found to be endothelium dependent and pressure and group independent. Furthermore, the change in tension induced by L-NNA appears significantly more pronounced in SHR than in LH rats (P < 0.05). 5. These results indicate that the common defect associated with hypertension appears to be linked to the endothelium through alpha-adrenoceptors and muscarinic receptors in both the Japanese and Lyon groups. However, SHR differs markedly from LH rats by having a higher developed tension in response to NA, this increased tension being counterbalanced by the release of nitric oxide, as observed in the presence of L-NNA.     

Reduction in extracellular Ca^2＋ attenuates endothelium-dependent relaxation more than nitroprussideinduced relaxation

Aim:

To quantitatively assess the effect of lowering external Ca²⁺ ([Ca²⁺]_o) on both endothelium-dependent and -independent relaxations in rabbit aorta.

Methods:

Isometric contractions and relaxations of isolated aortae were recorded. When assessing the effect of reduced [Ca²⁺]_o on relaxations, the normal [Ca²⁺]_o solution was substituted with one of the reduced [Ca²⁺]_o solutions for one aorta, while a paired aorta was replenished with normal [Ca²⁺]_o solution.

Results:

The extent of acetylcholine (ACh)-induced relaxation, which is dependent on an intact endothelium, is time-dependent, and inversely related to [Ca²⁺]_o in a range of 0.02–2 mmol/L. ACh-induced relaxations were not significantly altered by the magnitude of the precontraction induced by PGF_2α. Nitroprusside-induced relaxations, which are independent of the endothelium, are also attenuated by reduced [Ca²⁺]_o. Relaxant responses to ACh were significantly more susceptible to reduced [Ca²⁺]_o than nitroprusside-induced relaxations. A maximally effective relaxing concentration of D600, an L-type Ca channel blocker methoxyverapamil, (10⁻⁵ mol/L) attenuated ACh-induced relaxations, whereas nitroprusside-induced relaxations were unaffected by D600.

Conclusion:

Thus, endothelium-dependent relaxation is more dependent on [Ca²⁺]_o than endothelium-independent relaxation, and it seems likely that [Ca²⁺]_o plays an important role not only in contractile processes, but also in relaxant processes as well.     

金雀异黄素对正常的和过氧化氢损伤的内皮细胞的影响(英文)

目的 :观察金雀异黄素 (genistein)对体外培养的血管内皮细胞 (ECV 3 0 4)生长的影响和对过氧化氢引起ECV 3 0 4细胞损伤的保护作用。方法 :将ECV 3 0 4细胞与金雀异黄素 0 .1～ 1 0 0 μmol·L-1共同孵育 2 4～ 96h ,通过MTT法测定细胞存活率。为了观察金雀异黄素对过氧化氢引起ECV 3 0 4细胞损伤的保护作用 ,将细胞分成 3组 ,分别为对照组、过氧化氢损伤模型组和金雀异黄素治疗组 ,治疗组ECV 3 0 4细胞先与金雀异黄素 6.2 5～ 1 0 0 μmol·L-1共同孵育 3 0min ,然后模型组和治疗组ECV3 0 4细胞均加入过氧化氢 1 0mmol·L-1孵育 ,3 0min后以MTT法测定OD值 ,以此反映各组ECV 3 0 4的生存情况。结果 :金雀异黄素对于正常ECV 3 0 4细胞生长的作用与浓度和作用时间有关 ,浓度为1 0 0 μmol·L-1时 ,作用 2 4,48h能明显促进ECV3 0 4生长 (P <0 .0 1 ) ,而作用 96h则表现为明显的抑制作用 (P <0 .0 5 ) ;浓度为 1 0 μmol·L-1时 ,作用48,72h对ECV 3 0 4细胞生长也有促进作用 (P <0 .0 5 ) ;而当金雀异黄素浓度降低为 0 .1 ,1 μmol·L-1时 ,对ECV 3 0 4细胞生长无明显影响。过氧化氢 1 0mmol·L-1可使ECV 3 0 4的存活率明显下降(P <0 .0 5 ) ;预先给予金雀异黄素 2 5 ,5 0 ,1 0 0 μmol·L-1能浓度依赖性地     

Effects of calcium and potassium supplements on arterial tone in vitro in spontaneously hypertensive rats

1. Calcium and potassium intakes inversely correlate with blood pressure in experimental hypertension. Therefore, we examined the effects of calcium and potassium supplements alone and in combination on arterial tone in spontaneously hypertensive rats (SHR). Wistar-Kyoto (WKY) rats served as normotensive controls. Calcium and potassium contents in the control diet were both 1%, while those in supplemented chows were 3% and 3.5%, respectively. The sodium content of all diets was moderately elevated to 1.1%.
2. After 12 weeks of the study systolic blood pressures in SHR on high calcium and on high potassium diets were markedly lower (about 53 and 58 mmHg, respectively) than in hypertensive controls, while combined supplementation of these cations reduced blood pressure even further (about 69 mmHg).
3. Responses of mesenteric arterial rings in vitro were examined at the end of the study. Both high calcium and high potassium diets improved the impaired relaxation to acetylcholine (ACh) in SHR, while the combination of these supplements completely normalized this response. Cyclo-oxygenase inhibition by diclofenac augmented the relaxation to ACh in hypertensive controls but not in the other groups. Nevertheless, enhanced endothelium-mediated dilatation was still observed in the presence of diclofenac and the nitric oxide synthase inhibitor N^G-nitro-L-arginine methyl ester (L-NAME) in all supplemented groups. Interestingly, additional blockade of Ca²⁺-activated K⁺ channels by tetraethylammonium abolished the improved relaxation to ACh in SHR on high calcium and on high potassium, but distinct responses were still observed in WKY rats and SHR on the combined supplement.
4. When hyperpolarization of smooth muscle was prevented by precontraction of the preparations with 50 mM KCl, only marginal differences were observed in the diclofenac and L-NAME-resistant relaxations to ACh between the study groups. Finally, endothelium-independent vasorelaxations of noradrenaline-precontracted rings to nitroprusside, isoprenaline and cromakalim were comparably augmented by all supplements.
5. In conclusion, the vascular mechanisms underlying the antihypertensive effect of high calcium and high potassium diets during moderately elevated sodium intake in SHR may involve enhanced arterial hyperpolarization, increased smooth muscle sensitivity to nitric oxide and decreased production of vasoconstrictor prostanoids. The administration of these cations in combination was more effective than either of them alone in reducing blood pressure and restoring arterial tone.

     

金雀异黄素对低密度脂蛋白诱导的内皮细胞c-myc mRNA表达的影响(英文)

目的 :研究金雀异黄素对氧化型低密度脂蛋白诱导的人血管内皮细胞c mycmRNA表达的影响。方法 :低密度脂蛋白采用密度梯度超速离心法从健康人血浆中提取 ,经铜离子氧化制备成氧化型低密度脂蛋白。培养的人血管内皮细胞给予氧化型低密度脂蛋白 2 0 0mg·L- 1或同时给予金雀异黄素 10 0 μmol·L- 1诱导不同时间 (1,2 ,4h) ,提取细胞总RNA进行Northernblot杂交。结果 :2 0 0mg·L- 1氧化型低密度脂蛋白刺激内皮细胞c mycmR NA在 1h增加为对照水平的 3倍 ,2h增加为对照水平的 3.3倍 ,4h降到对照水平以下 ;给予氧化型低密度脂蛋白诱导的同时给予金雀异黄素 10 0 μmol·L- 1其c mycmRNA表达量在 1h为单独给予氧化型低密度脂蛋白诱导的 80 % ,2h为 6 0 %。结论 :金雀异黄素能有效抑制氧化型低密度脂蛋白诱导的人血管内皮细胞c mycmRNA表达增高     

激活补体对血小板的作用

目的：研究激活补体对血小板的作用和随后对血管内皮细胞和血管平滑肌细胞的作用．方法：用酵母多糖A激活补体观察血小板变形、凝血活酶表达和膜粘度的改变,观察酵母多糖A处理的富血小板血浆对内皮细胞和血管平滑肌细胞的生长、DNA含量和膜微粘度的影响．结果：酵母多糖A能引起富血小板血浆的血小板明显变形、膜微粘度增加和凝血活酶表达增加,但不引起经洗脱的血小板变形,新鲜的贫血小板血浆能恢复酵母多糖A引起的作用,但经眼镜蛇毒因子预处理后作用消失．酵母多糖A引起的血小板变形能被依他酸5mmol/L、Mn^2 10nmol/L、河豚毒素40μmol/L或吲哚美辛100μmol/L阻断．酵母多糖A处理的富血小板血浆上清液能抑制血管内皮细胞生长,但对血管平滑肌细胞生长有促进作用,促使血管平滑肌细胞进入G2期和M期,同时内浆网变粗和游离的核糖体出现,而内皮细胞的线粒体出现空泡．结论：激活补体引起血小板显著变形,损伤血管内皮细胞并使血管平滑肌细胞增殖．     

尼群地平单用及其与美多洛尔合用对大鼠血压和胸主动脉环收缩的影响

<正> 近年来,在高血压病的治疗中,钙拮抗剂(如硝苯啶)与β受体阻断剂(如醋丁洛尔)的合用已引起关注.尼群地平(nitrendIpine,Nit)是一种较新的二氢吡啶类钙通道阻滞剂,美多洛尔(metoprolol,Met)是一种选择性β_1受体阻断剂.该二药的合用尚未见研究报道.本文采用麻醉大鼠观察     

雌二醇对离体和在体气管平滑肌收缩活动的抑制作用

目的:研究雌二醇对离体和在体气管平滑肌收缩的作用.方法:(1)将家兔离体气管平滑肌条置于装有Krebs液的肌槽中温育,并通入95％O_2和5％CO_2的混合气体.二导记录仪记录肌条的等长张力.(2)测量肌注雌二醇(1mg/kg)前后乙酰胆碱和组胺引发豚鼠哮喘的潜伏期.结果:(1)雌二醇(100μmol/L)对乙酰胆碱和氯化钾诱发的收缩有明显的舒张作用(舒张百分比分别为39％±5％和45％±19％).其作用可被蚓哚美辛和亚甲蓝部分阻断(26％±8％和28％±13％),但不能被L-NNA、心得安和去除上皮所影响(舒张百分比分别为38％±10％,40％±15％,37％±8％).雌二醇能使乙酰胆碱及氯化钙的量效曲线明显右移(pD_2~′值分别为3.98和4.75).另外,雌二醇可明显抑制乙酰胆碱引起的第Ⅰ时相性收缩,对氯化钙引起的第Ⅱ时相性的收缩无明显影响.(2)肌注雌二醇(1mg/kg)可使豚鼠的引喘潜伏期明显延长.结论:(1)雌二醇对兔离体气管平滑肌的作用是非上皮依赖性的,与抑制电压依赖性钙通道和细胞内钙从内质网的释放有关,还部分与cGMP介导的松弛途径及刺激气道平滑肌释放前列腺素类物质有关,但与β-肾上腺素能受体介导的舒张无关.(2)雌二醇可明显舒张豚鼠在体气管平滑肌.     

重组人酸性成纤维生长因子对离体小鼠胸主动脉的弱缩血管作用及其机制

成纤维细胞生长因子(Fibroblast growth factors,FGFs)是一类广泛地促进来源于中胚层及神经外胚层细胞增殖的活性物质,近年来对其非促分裂效应不断受到广泛关注,特别是对血管张力的调节作用得到了人们的关注.     

藻酸双酯钠对大鼠离体去内皮胸主动脉环的舒缩作用

目的:观察藻酸双酯钠(polysaccharide sulfate,PSS)对离体大鼠胸主动脉平滑肌舒缩的影响。方法:采用大鼠离体去内皮主动脉环灌流模型,观察不同浓度PSS(5×10-2～5×102 mg.L-1)对基础状态及氯化钾(KCl)、去氧肾上腺素(PE)等试剂的血管收缩效应的影响。结果:不同浓度PSS对基础状态、KCl或PE的去内皮血管环收缩效应无明显影响。PSS(5×102 mg.L-1)对内钙释放及外钙内流引起的血管收缩效应无明显影响。结论:在5×10-2～5×102 mg.L-1浓度范围内,PSS对离体血管平滑肌没有明显舒缩作用。     

酪氨酸激酶抑制剂对cyclopiazoni cacid引起的大鼠主动脉血管环收缩效应的影响

目的　探讨酪氨酸激酶在Ca2 +池操纵性Ca2 +内流中的作用。方法　记录大鼠胸主动脉环收缩反应。结果　①不同剂量酪氨酸激酶抑制剂 genistein (1～ 10 0 μmol·L-1)和tyrphostin 2 5 (Tyr 2 5 ,1～ 30 μmol·L-1)均以浓度依赖性抑制cyclopiazonicacid (CPA)引起的平滑肌收缩平台期。Tyr 2 5的最大作用浓度为 10 μmol·L-1,抑制率为 42 %±11%。② 10 μmol·L-1Tyr 2 5和 1μmol·L-1nifedipine(Nif)对CPA引起电压依赖性Ca2 +通道 (VDCC)开放过程的抑制作用存在部分交叉。③ 1μmol·L-1Nif预处理阻断VDCC作用后 ,10 μmol·L-1Tyr 2 5只能部分阻断CPA引起的Ca2 +池操纵性Ca2 +通道 (SOCC)开放过程 ,再加入 6 0 μmol·L-1SK&F96 36 5可完全阻断SOCC的开放过程。结论　CPA引起平滑肌的收缩过程中 ,蛋白质酪氨酸激酶参与了开启VDCC和SOCC的信号转导过程     

自由基使血管舒张因子从主动脉内皮细胞与平滑肌细胞中释放(英文)

电解Krebs液产生自由基,灌流通过有内皮细胞或去内皮细胞的家兔主动脉;或通过生长在微粒上的小牛主动脉内皮细胞柱;用淋浴生物检定法均检测出由血管内皮细胞或血管平滑肌释放出的血管舒张因子。这种血管舒张因子与用ADP通过血管内皮细胞柱释放的血管内皮舒张因子(EDRF)有类似的性质,即作用时间短暂,并可被同时灌注N-硝基-L-精氨酸(为EDRF合成拮抗剂)或血红蛋白(为EDRF清除剂)所减弱。在去内皮细胞的主动脉,ADP的释放作用消失,但自由基的释放作用仍存在,表明血管平滑肌也可释放,因羟自由基消除剂水杨酸钠能明显减弱电解产生的自由基的这种释放作用,故推测电解产生的羟自由基在释放血管舒张因子中起主要作用。     

超氧阴离子对培养的牛动脉平滑肌细胞内钙及收缩性的影响

目的研究超氧阴离子对牛主动脉平滑肌细胞内钙及收缩性的影响。方法采用Ｆｕｒａ－２测定牛肺动脉平滑肌细胞内钙及采用胶原凝胶实验方法分析平滑肌细胞的收缩性。结果超氧阴离子作用于平滑肌细胞后使ＡＴＰ（１０μｍｏｌ·Ｌ－１）诱导的细胞内钙浓度的增加从（２０６± １０） ｎｍｏｌ·Ｌ－１降到（１４７±１５） ｎｍｏｌ·Ｌ－１。 ５ ｍｉｎ内细胞内钙浓度增加的积分（∫　△［Ｃａ２＋］ｉ·ｄｔ）从（１２．２± ０．５）μｍｏｌ· Ｌ－１·ｓ－１降至（９．８± ０．８）μｍｏｌ·Ｌ－１·ｓ－１。ｔｈａｐｓｉｇａｒｇｉｎ在无钙溶液中诱导的细胞内钙浓度的增加不受超氧阴离子的影响,而在含钙的Ｋｒｅｂａ溶液中,超氧阴离子能使随后的钙释放激活的钙进入（△［Ｃａ２＋］ｉＣＲＡＣ）从（２７．３ ±１．０） ｎｍｏｌ·Ｌ－１降到（１３．５ ±１．０） ｎｍｏｌ·Ｌ－１。ＡＴＰ诱导的凝胶面积减少的百分比从２４％±５％降到 ７．４％ ±０．２％;在无钙 Ｋｒｅｂｓ溶液中,ｔｈａｐｓｉｇａｒｇｉｎ诱导的凝胶面积减少的百分比从 ３．５％± ０．６％降到－０．５％±０．７％。结论超氧阴离子通过影响平滑肌细胞的内钙动员而降低它的收缩性。     

Dissociation between endothelium-mediated increases in tissue cGMP levels and modulation of aortic contractile responses

Summary Both methoxamine and clonidine elicited similar maximal contractions of rat isolated aorta in the absence of endothelium. These contractions were not associated with changes in tissue levels of cGMP or cAMP. In the presence of endothelium maximal methoxamine-induced contractions were not less than those elicited in the absence of endothelium but maximal clonidine-induced contractions were reduced to about 10% of those in the absence of endothelium. However, in the presence of endothelium both methoxamine and clonidine induced similar increases in tissue cGMP levels of about 1.5 to 2 fold; cAMP levels were unchanged. There is therefore a dissociation between endothelium-mediated inhibition of maximal contractile responses and increases in tissue levels of cGMP.     

Extraendothelial and constitutive COX‐2 expression is involved in the contractile effect of angiotensin II in the rat aorta

1 The role of the extraendothelial and constitutive isoforms of cyclo‐oxygenase‐2 (COX‐2) in the contractile effect of angiotensin II (Ang II) was investigated using thoracic and abdominal aortic rings without endothelium from young Wistar rats. 2 Ang II elicited similar contractions in both aortic segments, and the effect was inhibited by pretreatment with NS398 (a selective COX‐2 inhibitor) but not SC‐560 [selective cyclo‐oxygenase‐1 (COX‐1) inhibitor]. 3 COX‐2 mRNA was expressed under basal conditions in both aortic segments. Additionally, Ang II increased COX‐2 mRNA expression in the abdominal but not the thoracic segment, while cycloheximide (a protein synthesis inhibitor) did not affect the contractile response to Ang II in either of the two segments; this suggests that the effect is not associated with de novo COX‐2 synthesis. 4 In conclusion, the basal amount of COX‐2 found in aortic smooth muscle cells is sufficient to explain the production of the prostanoids related to the contractile effect of Ang II. The production of these prostanoids, which are derived from constitutive COX‐2, occurs independently of the endothelium vascular system.