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Endothelium-derived hyperpolarizing factor. 内皮衍生的超极化因子。
Pub Date : 1990-01-01 DOI: 10.1159/000158815
K Komori, P M Vanhoutte

Although nitric oxide appears to be the major endothelium-derived relaxing factor (EDRF), it cannot explain all endothelium-dependent responses of isolated arteries. Thus, acetylcholine causes an endothelium-dependent, transient hyperpolarization, which is due to the release from the endothelial cells of a diffusible substance (endothelium-derived hyperpolarizing factor, EDHF) other than nitric oxide. The muscarinic receptors on the endothelium that trigger the release of EDHF belong to the M1-muscarinic subtype, while those activating the liberation of EDRF are M2-muscarinic in nature. The importance of endothelium-dependent hyperpolarization varies among different blood vessels. The hyperpolarization, and the resulting relaxation caused by EDHF can be attributed to an increase in K+ conductance in the vascular smooth muscle. Although the nature of EDHF remains elusive, it may be a labile metabolic of arachidonic acid.

虽然一氧化氮似乎是主要的内皮源性松弛因子(EDRF),但它不能解释孤立动脉的所有内皮依赖性反应。因此,乙酰胆碱引起内皮依赖的瞬时超极化,这是由于内皮细胞释放出一种可扩散物质(内皮衍生的超极化因子,EDHF)而不是一氧化氮。内皮上触发EDHF释放的毒蕈碱受体属于m1毒蕈碱亚型,而激活EDRF释放的毒蕈碱受体本质上属于m2毒蕈碱亚型。内皮依赖性超极化的重要性在不同的血管中有所不同。EDHF引起的超极化和由此引起的松弛可归因于血管平滑肌中K+电导的增加。虽然EDHF的性质尚不清楚,但它可能是花生四烯酸的一种不稳定代谢。
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引用次数: 52
EDRF in intact vascular networks. 完整血管网中的EDRF。
Pub Date : 1990-01-01 DOI: 10.1159/000158814
T M Griffith, D H Edwards

X-ray microangiography was used to investigate the role of basal EDRF activity in the isolated rabbit ear, changes in perfusion pressure at different flow rates being correlated with simultaneous changes in diameter in resistance arteries 70-1,000 microns in size. Under conditions of controlled-pressure but not controlled-flow perfusion the preparations were shown to autoregulate flow, but only when EDRF activity was inhibited by haemoglobin or L-NMMA. The diameter data indicated that this phenomenon was mediated by a flow- and/or pressure-dependent constrictor response that is normally suppressed by EDRF activity. We also investigated the influence of basal EDRF activity on the geometrical 'optimality' of resistance artery branching, using four models which minimise respectively the total surface area, volume, shear stress (drag) or power losses at bifurcations. EDRF activity was found to maintain optimality in terms of minimum volume and power losses over a wide range of flow rates in pharmacologically constricted preparations. This may allow rapid changes in flow to occur with only small changes in central arterial pressure and also help to minimise cardiac work.

x线显微血管造影研究了离体兔耳基底EDRF活性的作用,不同流速下灌注压力的变化与70-1,000微米的阻力动脉直径同时变化相关。在控制压力而非控制流量的灌注条件下,只有当血红蛋白或L-NMMA抑制EDRF活性时,这些制剂才能自动调节流量。直径数据表明,这种现象是由流量和/或压力相关的收缩反应介导的,这种反应通常被EDRF活性抑制。我们还研究了基础EDRF活动对阻力动脉分支几何“最优性”的影响,使用了四种模型,分别最小化总表面积,体积,切应力(阻力)或分岔时的功率损失。研究发现,在药理学收缩的制剂中,EDRF活性在大范围流速下的最小体积和功率损失方面保持最佳。这可能使血流发生快速变化,而中央动脉压变化很小,也有助于减少心脏工作。
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引用次数: 6
Vasoactive peptides and their receptors. 血管活性肽及其受体。
Pub Date : 1990-01-01 DOI: 10.1159/000158804
D Regoli, S Dion, N E Rhaleb, G Drapeau, P D'Orléans-Juste

Peptides act as vasoconstrictors (for instance angiotensins, vasopressin) or vasodilators (the kinins, the neurokinins), both through direct activation of specific receptors in the vascular smooth muscles or indirectly through the release of other endogenous inhibitors of the vascular tone. Kinins and neurokinins as well as their multiple receptors have been analyzed in the present study to assess the possible contributions of peptides to vasodilatation. Kinin receptors, B1 and B2, have been characterized, using new selective agonists and antagonists. B1 and B2 receptors appear to present in endothelium (B2) and in smooth muscles (B2, B1) of a variety of isolated vessels of the dog and the rabbit, where they subserve both stimulatory and inhibitory effects. Vasodilator inhibitory mechanisms depend on the release of the endothelium-relaxing factor and/or of prostanoids from the endothelium or the smooth muscles, especially in the dog renal vessels, where both B1 and B2 receptors appear to be involved in causing vasodilatation. B2 receptors have also been shown to activate cardiovascular reflexes through a direct action on sensory fibers or on reflexogenic areas of the epicardium. Three types of receptors for neurokinins, namely NK-1, NK-2 and NK-3, have been identified by the use of naturally occurring peptides and of some analogues that act as selective agonists of a single receptor type. NK-1 receptors (particularly sensitive to substance P) have been shown to be present in endothelia where they promote the release of the endothelium relaxing factor, while NK-2 receptors (sensitive to neurokinin A) are found in the pulmonary artery of the rabbit and act directly to contract the smooth muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

多肽作为血管收缩剂(如血管紧张素、血管加压素)或血管舒张剂(血管收缩素、神经收缩素),通过直接激活血管平滑肌中的特定受体或间接通过释放其他内源性血管张力抑制剂。本研究分析了激肽和神经激肽及其多种受体,以评估多肽对血管舒张的可能贡献。利用新的选择性激动剂和拮抗剂,已经对激肽受体B1和B2进行了表征。B1和B2受体存在于犬和兔多种离体血管的内皮(B2)和平滑肌(B2, B1)中,在那里它们具有刺激和抑制作用。血管舒张剂抑制机制依赖于内皮松弛因子和/或前列腺素从内皮或平滑肌的释放,特别是在狗肾血管中,B1和B2受体似乎都参与引起血管舒张。B2受体也被证明通过直接作用于感觉纤维或心外膜反射区来激活心血管反射。三种类型的神经激肽受体,即NK-1, NK-2和NK-3,已经通过使用天然存在的肽和一些类似物作为单一受体类型的选择性激动剂被鉴定出来。NK-1受体(对P物质特别敏感)已被证明存在于内皮中,它们促进内皮松弛因子的释放,而NK-2受体(对神经激肽A敏感)存在于兔的肺动脉中,并直接作用于平滑肌收缩。(摘要删节250字)
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引用次数: 22
Patterns of internal elastic lamina morphology in the canine common carotid artery. 犬颈总动脉内弹性板形态。
Pub Date : 1990-01-01 DOI: 10.1159/000158791
K J Hutchison, E J Sanders

The internal elastic lamina (IEL) of normal canine carotid arteries was examined by scanning electron microscopy in pressure-fixed specimens with intact endothelium. IEL appearance showed a marked variation between animals and was classified into fenestrated sheet, fibrous, and mixed varieties. This interpretation of the apparent morphology was confirmed with transmission electron microscopy. It was clear that IEL fenestrae were associated with surface depressions and that in areas of fibrous IEL there was surface elevation over individual fibres. Within individual animals there was little variation in the pattern of IEL either along or between common carotid arteries. If theories of atherogenesis involving the IEL are correct, the variation of IEL patterns between animals would suggest a corresponding variation of incidence and severity of atheromatous lesions of the common carotid artery between animals. Further, the occurrence of fibrous areas distributed throughout the fenestrated sheet would suggest a focal distribution of lesions along such arteries.

用扫描电镜对正常犬颈动脉内弹性层(IEL)进行了观察。IEL外观在动物间差异明显,可分为开孔片状、纤维状和混合型。透射电镜证实了这种对表面形貌的解释。很明显,IEL开窗与表面凹陷有关,在纤维性IEL区域,个别纤维表面升高。在单个动物中,沿颈总动脉或颈总动脉之间的IEL模式几乎没有变化。如果涉及IEL的动脉粥样硬化理论是正确的,动物之间IEL模式的差异将提示动物之间颈总动脉粥样硬化病变的发生率和严重程度的相应差异。此外,纤维区分布在整个开孔片的出现表明病变沿这些动脉有局灶性分布。
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引用次数: 5
Endothelium-dependent relaxations and chronic vasospasm after subarachnoid hemorrhage. 蛛网膜下腔出血后内皮依赖性松弛和慢性血管痉挛。
Pub Date : 1990-01-01 DOI: 10.1159/000158818
P Kim, P M Vanhoutte

Endothelium-dependent relaxations are abolished in the canine basilar artery after subarachnoid hemorrhage. However, the release of endothelium-derived relaxing factor (EDRF) toward the lumen is not reduced. These findings suggest that the responsiveness of the smooth muscle to EDRF is impaired during chronic vasospasm after subarachnoid hemorrhage.

蛛网膜下腔出血后,犬基底动脉内皮依赖性松弛消失。然而,内皮源性松弛因子(EDRF)向管腔的释放并未减少。这些发现表明,在蛛网膜下腔出血后的慢性血管痉挛期间,平滑肌对EDRF的反应性受损。
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引用次数: 9
Decreased activity of the sodium-calcium exchanger in tail artery of stroke-prone spontaneously hypertensive rats. 卒中易感自发性高血压大鼠尾动脉钠钙交换器活性降低。
Pub Date : 1990-01-01 DOI: 10.1159/000158810
L E Thompson, G J Rinaldi, D F Bohr

The ability of the Na-Ca exchanger to modify vascular relaxation was studied in rings isolated from tail arteries of stroke-prone spontaneously hypertensive rats (SHRSP) and normotensive Wistar-Kyoto rats (WKY). The arteries were contracted with norepinephrine (NE) 1 microM and after stabilization they were transferred to a Ca-free physiological salt solution still in presence of NE. The time to 50% relaxation (T-50) in these conditions was significantly greater in SHRSP (78 +/- 7 s) than in WKY (50 +/- 7 s). When the calcium pump was stopped with vanadate (VAN), the Ca uptake by the sarcoplasmic reticulum with ryanodine (RY) and the Na-Ca exchanger with a Na-free PSS, the relaxation was slowed (T-50 increased to 198 +/- 16 s in SHRSP and to 162 +/- 14 s in WKY). Releasing the Na-Ca exchanger only (i.e. still with VAN and RY but with normal Na in the bath) the T-50 for relaxation in Ca-free PSS was, in WKY, nearly as fast as in control conditions (54 +/- 8 s). However, the Na-Ca exchanger in SHRSP was not so effective, and the T-50 for relaxation was slower than in control conditions (122 +/- 10 s). We conclude that the activity of the Na-Ca exchanger is depressed in tail arteries of SHRSP. This abnormality in resistance vessels, would contribute to the enhanced vascular tone present in hypertension.

在脑卒中易感自发性高血压大鼠(SHRSP)和正常Wistar-Kyoto大鼠(WKY)的尾动脉环中,研究了Na-Ca交换剂改变血管舒张的能力。用1微米的去甲肾上腺素(NE)收缩动脉,稳定后将其转移到仍有NE存在的无ca生理盐溶液中。在这些条件下,SHRSP (78 +/- 7 s)达到50%弛豫时间(T-50)明显大于WKY (50 +/- 7 s)。当钙泵用钒酸盐(VAN)停止,肌浆网用ryanodine (RY)和Na-Ca交换剂用无na PSS时,弛豫时间(T-50)增加到SHRSP的198 +/- 16 s, WKY的162 +/- 14 s)减慢。在无ca的PSS中,仅释放Na- ca交换剂(即仍有VAN和RY,但槽内Na正常),在WKY中,Na- ca交换剂的弛豫T-50几乎与对照组一样快(54 +/- 8 s),而在SHRSP中Na- ca交换剂的弛豫T-50则不如对照组有效(122 +/- 10 s)。我们得出结论,SHRSP尾动脉中Na- ca交换剂的活性被抑制。这种阻力血管的异常会导致高血压时血管张力的增强。
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引用次数: 14
G-proteins and endothelial responses. g蛋白与内皮反应。
Pub Date : 1990-01-01 DOI: 10.1159/000158813
N A Flavahan, P M Vanhoutte

G-proteins are transducing proteins that couple a large number of membrane-bound receptors to a variety of intracellular effector systems. Pertussis toxin ADP-ribosylates certain G-proteins causing inhibition of their function. In porcine coronary arteries, pertussis toxin inhibited the endothelium-dependent relaxations evoked by alpha-2-adrenergic or serotonergic receptor stimulation, and by aggregating platelets or thrombin. Relaxations to nitric oxide and endothelium-dependent relaxations to bradykinin, adenosine diphosphate or A23187 were unaffected by the toxin. Therefore, certain endothelium-dependent relaxations are mediated by activation of a pertussis toxin-sensitive G-protein in the endothelial cells, most likely Gi-protein. In porcine coronary arteries with regenerated endothelium (following in vivo denudation), the endothelium-dependent relaxations caused by the pertussis toxin-sensitive stimuli were reduced and were not further affected by pertussis toxin. Relaxations to the other stimuli were not altered by the regeneration process and were still not affected by the toxin. In regenerating endothelial cells there may be a selective impairment of the G-protein-dependent mechanism for releasing EDRF, which may predispose the blood vessel to vasospasm or the initiation of vascular disease.

g蛋白是将大量膜结合受体偶联到多种细胞内效应系统的转导蛋白。百日咳毒素adp -核糖基化某些g蛋白,使其功能受到抑制。在猪冠状动脉中,百日咳毒素抑制由α -2-肾上腺素能或血清素能受体刺激以及血小板或凝血酶聚集引起的内皮依赖性松弛。对一氧化氮的松弛和对缓激肽、二磷酸腺苷或A23187的内皮依赖性松弛不受毒素影响。因此,某些内皮依赖性松弛是由内皮细胞中百日咳毒素敏感的g蛋白激活介导的,最有可能是gi蛋白。在再生内皮的猪冠状动脉中(在体内剥落后),百日咳毒素敏感刺激引起的内皮依赖性松弛减少,并且不受百日咳毒素的进一步影响。对其他刺激的松弛不受再生过程的影响,也不受毒素的影响。在再生内皮细胞中,释放EDRF的g蛋白依赖机制可能存在选择性损伤,这可能使血管易发生血管痉挛或引发血管疾病。
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引用次数: 66
Impaired dilatation of cerebral arterioles in chronic hypertension. 慢性高血压患者脑小动脉扩张受损。
Pub Date : 1990-01-01 DOI: 10.1159/000158817
D D Heistad, W G Mayhan, P Coyle, G L Baumbach

Several mechanisms impair cerebral vasodilatation during chronic hypertension. First, the external diameter of cerebral arterioles is reduced during chronic hypertension by structural 'remodeling'. Thus, both vascular hypertrophy and remodeling result in encroachment on the lumen. Second, endothelium-dependent dilatation of cerebral vessels is impaired during chronic hypertension. Third, blood flow through cerebral collaterals is impaired by chronic hypertension, so that an important compensatory mechanism is compromised. Impaired vasodilator responses, together with limitation of increases in collateral blood flow, may predispose to cerebral ischemia and stroke during chronic hypertension.

几种机制损害慢性高血压期间脑血管舒张。首先,在慢性高血压期间,脑小动脉外径通过结构“重塑”而减小。因此,血管肥大和重构都导致管腔的侵犯。其次,慢性高血压期间脑血管内皮依赖性扩张受损。第三,慢性高血压损害了脑络的血流量,从而损害了一个重要的代偿机制。血管舒张反应受损,加上侧枝血流量增加受限,可能易导致慢性高血压患者脑缺血和脑卒中。
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引用次数: 68
The first Robert Furchgott lecture: from endothelium-dependent relaxation to the L-arginine:NO pathway. 第一个Robert Furchgott讲座:从内皮依赖性松弛到l -精氨酸:NO途径。
Pub Date : 1990-01-01 DOI: 10.1159/000158812
S Moncada

Nitric oxide (NO) is released from vascular endothelial cells and fresh vascular tissue in amounts sufficient to account for the biological actions of endothelium-derived relaxing factor. It is synthesized from the terminal guanidino nitrogen atom(s) of L-arginine, a process that is inhibited by NG-monomethyl-L-arginine (L-NMMA). Studies using L-NMMA have shown that NO is constantly generated by the vessel wall to maintain vasodilator tone. The L-arginine:NO pathway has now been identified in a number of other cells and tissues, in many of which it acts as the transduction mechanism for stimulation of the soluble guanylate cyclase.

一氧化氮(NO)从血管内皮细胞和新鲜血管组织中释放,其数量足以解释内皮源性松弛因子的生物作用。它是由l-精氨酸的末端胍基氮原子合成的,该过程被ng -单甲基- l-精氨酸(L-NMMA)抑制。使用L-NMMA的研究表明,血管壁不断产生NO以维持血管舒张剂的张力。l -精氨酸:NO途径现已在许多其他细胞和组织中被发现,在许多细胞和组织中,它作为刺激可溶性鸟苷酸环化酶的转导机制。
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引用次数: 46
Nonpeptide angiotensin II receptor antagonists: a novel class of antihypertensive agents. 非肽血管紧张素II受体拮抗剂:一类新的抗高血压药物。
Pub Date : 1990-01-01 DOI: 10.1159/000158821
P B Timmermans, D J Carini, A T Chiu, J V Duncia, W A Price, G J Wells, P C Wong, R R Wexler, A L Johnson

The most direct approach to block the function of the renin-angiotensin system would be to antagonize angiotensin II (AII) at the level of its receptor. However, the AII receptor antagonists currently available, such as saralasin, are peptides which still retain agonistic activity and lack oral bioavailability. We have identified the N-benzylimidazoles, S-8307 and S-8308, as weak, but selective nonpeptide AII receptor antagonists. These initial leads were subsequently converted into more potent compounds, such as EXP6155, EXP6803 and EXP7711, while maintaining the selectivity. The compounds displace 3H-AII from its specific binding sites in adrenal cortical membranes and smooth muscle cells. They competitively inhibit the vasoconstrictor response to AII in various in vivo and in vitro preparations, but do not influence those to KCl, norepinephrine, and vasopressin. Converting enzyme and renin are not affected by these agents. In renal hypertensive rats and sodium-depleted dogs our compounds cause a sustained decrease in arterial pressure following intravenous and oral (EXP7711) administration, and are devoid of agonistic properties. Taken together, these nonpeptide structures are true competitive AII receptor antagonists and represent a new class of effective antihypertensive agents.

阻断肾素-血管紧张素系统功能的最直接方法是在受体水平上拮抗血管紧张素II (AII)。然而,目前可用的AII受体拮抗剂,如saralasin,是仍然保留激动活性且缺乏口服生物利用度的肽。我们已经确定n -苄基咪唑,S-8307和S-8308是弱的,但选择性的非肽AII受体拮抗剂。这些初始先导物随后被转化为更有效的化合物,如EXP6155、EXP6803和EXP7711,同时保持了选择性。这些化合物取代3H-AII在肾上腺皮质膜和平滑肌细胞中的特定结合位点。在各种体内和体外制剂中,它们竞争性地抑制血管收缩剂对AII的反应,但不影响对KCl、去甲肾上腺素和抗利尿激素的反应。转化酶和肾素不受这些药物的影响。在肾性高血压大鼠和钠耗尽犬中,我们的化合物在静脉和口服(EXP7711)给药后可持续降低动脉压,并且不具有激动剂特性。综上所述,这些非肽结构是真正的竞争性AII受体拮抗剂,代表了一类新的有效抗高血压药物。
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引用次数: 16
期刊
Blood vessels
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