Pub Date : 1996-01-01DOI: 10.3109/10623329609024676
S. Taddei
Endothelium plays a key role in modulating vascular tone through the production of vasodilator and vasoconstrictor substances. In animals, experimental hypertension is associated with endothelial dysfunction. In human hypertension, available evidence indicates the presence of a reduced basal production of nitric oxide and of an impaired vasodilation to the endothelium-dependent agonist acetylcholine or to the chemically related methacholine in the forearm and coronary vasculature. This abnormal response to endothelium-dependent agonists seems to be caused by the simultaneous presence of an alteration in the L-arginine-nitric oxide pathway and the production of cyclooxygenase-derived constrictor prostanoids. The reduced basal production of nitric oxide seems to be secondary to blood pressure increase while, at variance with observations in animals, it is possible that the impaired agonist-evoked endothelium-dependent vasodilation could be a primary phenomenon since it can be detected in young normotensive ...
{"title":"Endothelium-Dependent Vasodilation in Hypertensive Patients","authors":"S. Taddei","doi":"10.3109/10623329609024676","DOIUrl":"https://doi.org/10.3109/10623329609024676","url":null,"abstract":"Endothelium plays a key role in modulating vascular tone through the production of vasodilator and vasoconstrictor substances. In animals, experimental hypertension is associated with endothelial dysfunction. In human hypertension, available evidence indicates the presence of a reduced basal production of nitric oxide and of an impaired vasodilation to the endothelium-dependent agonist acetylcholine or to the chemically related methacholine in the forearm and coronary vasculature. This abnormal response to endothelium-dependent agonists seems to be caused by the simultaneous presence of an alteration in the L-arginine-nitric oxide pathway and the production of cyclooxygenase-derived constrictor prostanoids. The reduced basal production of nitric oxide seems to be secondary to blood pressure increase while, at variance with observations in animals, it is possible that the impaired agonist-evoked endothelium-dependent vasodilation could be a primary phenomenon since it can be detected in young normotensive ...","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"40 1","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80534015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1996-01-01DOI: 10.3109/10623329609024692
S. Götze, W. Auch‐Schwelk, E. Duske, E. Fleck
Cyclosporine A is an efficient immunosuppressive agent, however, its use is associated with complex alterations of vascular tone. Numerous clinical and experimental observations indicate acute and chronic effects of cyclosporine A that are modulating endothelial and vascular smooth muscle function. Cyclosporine A impairs the vasodilator function of the endothelium; at the vascular smooth muscle contractions to angiotensin II are augmented, whereas conflicting results were obtained with other vasoconstrictors. Furthermore, cyclosporine A may alter circulating and locally released vasoactive hormons, such as renin/angiotensin II, catecholamines and endothelin-1. The cellular mechanisms mediating the effects of cyclosporine A in the arterial wall are not completely understood, but several experimental findings give a more and more detailed picture of potentially involved systems.
{"title":"Regulation of Vascular Tone during Treatment with Cyclosporine A: Modulation of Endothelial and Vascular Smooth Muscle Function","authors":"S. Götze, W. Auch‐Schwelk, E. Duske, E. Fleck","doi":"10.3109/10623329609024692","DOIUrl":"https://doi.org/10.3109/10623329609024692","url":null,"abstract":"Cyclosporine A is an efficient immunosuppressive agent, however, its use is associated with complex alterations of vascular tone. Numerous clinical and experimental observations indicate acute and chronic effects of cyclosporine A that are modulating endothelial and vascular smooth muscle function. Cyclosporine A impairs the vasodilator function of the endothelium; at the vascular smooth muscle contractions to angiotensin II are augmented, whereas conflicting results were obtained with other vasoconstrictors. Furthermore, cyclosporine A may alter circulating and locally released vasoactive hormons, such as renin/angiotensin II, catecholamines and endothelin-1. The cellular mechanisms mediating the effects of cyclosporine A in the arterial wall are not completely understood, but several experimental findings give a more and more detailed picture of potentially involved systems.","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"20 1","pages":"159-169"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83194842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1996-01-01DOI: 10.3109/10623329609024680
J. An, T. Okamura, A. Mori, N. Toda
Endothelin (ET)-1 and ET-3 elicited relaxations at 1 nM and contractions at 10 nM or higher, whereas IRL1620 induced only relaxation in dog pulmonary arteries. The relaxations by ET-1, ET-3 and IRL1620 were not affected by indomethacin, but were abolished by endothelium denudation or NG-nitro-L-arginine. The relaxations caused by ET-3 and IRL1620 were markedly suppressed by IRL1038. BQ123 potentiated ET-1-, ET-3- and IRL1620-induced relaxations and markedly suppressed ET-1- and ET-3-induced contractions. ET-1, ET-3 and IRL1620 produced only contraction in pulmonary venous strips; the order of potency was ET-1 > ET-3 > IRL1620. The contraction induced by ET-1 was markedly suppressed by BQ123. This ETA antagonist also suppressed the ET-3-induced contraction. Under ETA receptor blockade, EŤ-3 (30 nM) produced endothelium-independent relaxation, which was abolished by indomethacin. IRL1038 suppressed the IRL1620-induced contraction. It is concluded that pulmonary arterial and venous responses to ET can be att...
{"title":"Canine Pulmonary Arterial and Venous Responses Mediated by Endothelin ETA and ETB Receptors","authors":"J. An, T. Okamura, A. Mori, N. Toda","doi":"10.3109/10623329609024680","DOIUrl":"https://doi.org/10.3109/10623329609024680","url":null,"abstract":"Endothelin (ET)-1 and ET-3 elicited relaxations at 1 nM and contractions at 10 nM or higher, whereas IRL1620 induced only relaxation in dog pulmonary arteries. The relaxations by ET-1, ET-3 and IRL1620 were not affected by indomethacin, but were abolished by endothelium denudation or NG-nitro-L-arginine. The relaxations caused by ET-3 and IRL1620 were markedly suppressed by IRL1038. BQ123 potentiated ET-1-, ET-3- and IRL1620-induced relaxations and markedly suppressed ET-1- and ET-3-induced contractions. ET-1, ET-3 and IRL1620 produced only contraction in pulmonary venous strips; the order of potency was ET-1 > ET-3 > IRL1620. The contraction induced by ET-1 was markedly suppressed by BQ123. This ETA antagonist also suppressed the ET-3-induced contraction. Under ETA receptor blockade, EŤ-3 (30 nM) produced endothelium-independent relaxation, which was abolished by indomethacin. IRL1038 suppressed the IRL1620-induced contraction. It is concluded that pulmonary arterial and venous responses to ET can be att...","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"38 1","pages":"41-49"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84610303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1996-01-01DOI: 10.3109/10623329609024694
H. Zoellner, E. Bielek, E. Vanyek, A. Fabry, J. Wojta, Manfred Höfler, B. Binder
Apoptosis of endothelial cells (EC) is responsible for the removal of blood vessels during vascular remodelling. Cultured human umbilical vein EC (HUVEC) undergo apoptosis if deprived of either serum or adhesion. Apoptotic HUVEC rapidly loose adhesion and in this paper we describe the ultrastructure of detached apoptotic HWEC and human microvascular EC (HMEC). These cells displayed the formation of apoptotic bodies, nuclear condensation and nuclear fragmentation typical of apoptosis in other cell types. Ultrastructural changes occurred in parallel with the internucleosomal DNA cleavage characteristic of apoptosis. An important difference between apoptotic HWEC and other reported cells was the formation of vesicle-like canalicular structures confluent with the plasma membrane surface. These structures formed an interconnecting network throughout the apoptotic cell. Apoptotic HMEC also displayed this canalicular pattern. Continuity of the plasma membrane surface of apoptotic EC with these canaliculi was est...
{"title":"Canalicular Fragmentation of Apoptotic Human Endothelial Cells","authors":"H. Zoellner, E. Bielek, E. Vanyek, A. Fabry, J. Wojta, Manfred Höfler, B. Binder","doi":"10.3109/10623329609024694","DOIUrl":"https://doi.org/10.3109/10623329609024694","url":null,"abstract":"Apoptosis of endothelial cells (EC) is responsible for the removal of blood vessels during vascular remodelling. Cultured human umbilical vein EC (HUVEC) undergo apoptosis if deprived of either serum or adhesion. Apoptotic HUVEC rapidly loose adhesion and in this paper we describe the ultrastructure of detached apoptotic HWEC and human microvascular EC (HMEC). These cells displayed the formation of apoptotic bodies, nuclear condensation and nuclear fragmentation typical of apoptosis in other cell types. Ultrastructural changes occurred in parallel with the internucleosomal DNA cleavage characteristic of apoptosis. An important difference between apoptotic HWEC and other reported cells was the formation of vesicle-like canalicular structures confluent with the plasma membrane surface. These structures formed an interconnecting network throughout the apoptotic cell. Apoptotic HMEC also displayed this canalicular pattern. Continuity of the plasma membrane surface of apoptotic EC with these canaliculi was est...","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"28 1","pages":"177-188"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90523029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1996-01-01DOI: 10.3109/10623329609024704
M. Mutin, F. George, G. Lesaule, J. Sampol
To obtain viable single-cell suspensions for flow cytometry analysis, endothelial cells are usually harvested by using a solution of trypsin-EDTA or PBS-EDTA alone. Trypsin is known to alter antigenic epitopes and thus may lead to an inaccurate assessment of cell-surface molecule expression. First it was determined that the best viable cell recovery was obtained with trypsin-EDTA compared to alternative methods, i.e., cell scraper, EDTA and a cell-dissociation solution. After cell detachment with trypsin-EDTA of increasing concentrations and incubation times and indirect immunolabeling with monoclonal antibodies, flow cytometry analysis of endothelial cell antigen expression established that a solution of 0.05% trypsin-0.02% EDTA incubated for 0.5 min yielded endothelial cells whose integrity of antigenic expression was maintained. The following cell-surface molecules were studied: S-Endo 1 antigen, CD54 ([CAM-]), Thrombomodulin (TM), CD31 (PECAM-I), CD49b (VLAa2) and CD51 (VNRa).
{"title":"Reevaluation of Trypsin-EDTA for Endothelial Cell Detachment before Flow Cytometry Analysis","authors":"M. Mutin, F. George, G. Lesaule, J. Sampol","doi":"10.3109/10623329609024704","DOIUrl":"https://doi.org/10.3109/10623329609024704","url":null,"abstract":"To obtain viable single-cell suspensions for flow cytometry analysis, endothelial cells are usually harvested by using a solution of trypsin-EDTA or PBS-EDTA alone. Trypsin is known to alter antigenic epitopes and thus may lead to an inaccurate assessment of cell-surface molecule expression. First it was determined that the best viable cell recovery was obtained with trypsin-EDTA compared to alternative methods, i.e., cell scraper, EDTA and a cell-dissociation solution. After cell detachment with trypsin-EDTA of increasing concentrations and incubation times and indirect immunolabeling with monoclonal antibodies, flow cytometry analysis of endothelial cell antigen expression established that a solution of 0.05% trypsin-0.02% EDTA incubated for 0.5 min yielded endothelial cells whose integrity of antigenic expression was maintained. The following cell-surface molecules were studied: S-Endo 1 antigen, CD54 ([CAM-]), Thrombomodulin (TM), CD31 (PECAM-I), CD49b (VLAa2) and CD51 (VNRa).","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"15 1","pages":"289-295"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86745811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1996-01-01DOI: 10.3109/10623329609024702
Baichun Yang, L. Chen, J. Mehta
Aggregating platelets cause relaxation of precontracted vascular tissues with intact endothelium. To determine the modulation of vasorelaxation by lipoprotein-rich platelets, rat platelets were preincubated with buffer, native low density lipoprotein (n-LDL, 100 μg protein/ml), oxidized LDL (ox-LDL, 100 μg protein/ml) or high density lipoprotein (HDL, 100 μg protein/ml) at 37°C for 1 hour, washed twice, and then suspended into organ baths containing precontracted endothelium-intact rat aortic rings. While all platelet preparations caused relaxation of rat aortic rings, the magnitude of relaxation induced by ox-LDL-treated platelets was less than that by buffer-treated platelets (p < 0.05). Pretreatment of platelets with native LDL or HDL did not affect the magnitude of vasorelaxation. Treatment of platelets with the cyclooxygenase inhibitor indomethacin (5 × 10−5 M) did not affect the attenuated vasorelaxation in response to ox-LDL-treated platelets. Pretreatment of aortic rings with the thromboxane (TX) ...
{"title":"Attenuation of Platelet-Induced Vasorelaxation by Pretreatment of Platelets with Oxidized Low Density Lipoproteins: Important Role of Serotonin","authors":"Baichun Yang, L. Chen, J. Mehta","doi":"10.3109/10623329609024702","DOIUrl":"https://doi.org/10.3109/10623329609024702","url":null,"abstract":"Aggregating platelets cause relaxation of precontracted vascular tissues with intact endothelium. To determine the modulation of vasorelaxation by lipoprotein-rich platelets, rat platelets were preincubated with buffer, native low density lipoprotein (n-LDL, 100 μg protein/ml), oxidized LDL (ox-LDL, 100 μg protein/ml) or high density lipoprotein (HDL, 100 μg protein/ml) at 37°C for 1 hour, washed twice, and then suspended into organ baths containing precontracted endothelium-intact rat aortic rings. While all platelet preparations caused relaxation of rat aortic rings, the magnitude of relaxation induced by ox-LDL-treated platelets was less than that by buffer-treated platelets (p < 0.05). Pretreatment of platelets with native LDL or HDL did not affect the magnitude of vasorelaxation. Treatment of platelets with the cyclooxygenase inhibitor indomethacin (5 × 10−5 M) did not affect the attenuated vasorelaxation in response to ox-LDL-treated platelets. Pretreatment of aortic rings with the thromboxane (TX) ...","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"41 1","pages":"273-279"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73353812","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1996-01-01DOI: 10.3109/10623329609024686
D. Faller, Hillary F. Barnett, R. Weisbrod, R. Cohen
Nitric oxide is synthesized by vascular smooth muscle cells in response to endotoxin or inflammatory mediators. We investigated the molecular basis for the induction of nitric oxide synthase (NOS) in response to lipopolysaccharide (LPS) or IL-1β using rat vascular smooth muscle cells derived from pulmonary and systemic vasculature. The regulation of mRNA levels for this enzyme in response to LPS or IL-1β treatment was examined in parallel with changes in levels of cyclic GMP. We found an increase in expression of inducible NOS transcript corresponding to an increase in cyclic GMP levels beginning with 3 hr of exposure to either LPS or IL-Iβ. In cells derived from the pulmonary circulation, initial induction of NOS transcript was detectable at 3 hr and the transcript levels continued to increase to a maximum level at 24 hr. In contrast, the cells derived from the systemic vasculature showed a maximal induction of NOS transcript at 3 hr, and the level decreased from this time point to 24 hr. The full induct...
一氧化氮是由血管平滑肌细胞对内毒素或炎症介质的反应合成的。我们利用大鼠肺和全身血管平滑肌细胞，研究了一氧化氮合酶(NOS)对脂多糖(LPS)或IL-1β反应的分子基础。该酶的mRNA水平在LPS或IL-1β处理下的调节与环GMP水平的变化同时进行了研究。我们发现，从暴露于LPS或il - i - β 3小时开始，诱导型NOS转录物的表达增加，与循环GMP水平的增加相对应。在来源于肺循环的细胞中，NOS转录物的初始诱导在3小时可检测到，转录物水平在24小时继续增加到最高水平。相比之下，来自全身血管的细胞在3小时时表现出最大的NOS转录物诱导，从这个时间点到24小时水平下降。完整的归纳…
{"title":"Regulation of Nitric Oxide Synthase Induction in Cultured Vascular Smooth Muscle Cells by Lipopolysaccharide and Interferon","authors":"D. Faller, Hillary F. Barnett, R. Weisbrod, R. Cohen","doi":"10.3109/10623329609024686","DOIUrl":"https://doi.org/10.3109/10623329609024686","url":null,"abstract":"Nitric oxide is synthesized by vascular smooth muscle cells in response to endotoxin or inflammatory mediators. We investigated the molecular basis for the induction of nitric oxide synthase (NOS) in response to lipopolysaccharide (LPS) or IL-1β using rat vascular smooth muscle cells derived from pulmonary and systemic vasculature. The regulation of mRNA levels for this enzyme in response to LPS or IL-1β treatment was examined in parallel with changes in levels of cyclic GMP. We found an increase in expression of inducible NOS transcript corresponding to an increase in cyclic GMP levels beginning with 3 hr of exposure to either LPS or IL-Iβ. In cells derived from the pulmonary circulation, initial induction of NOS transcript was detectable at 3 hr and the transcript levels continued to increase to a maximum level at 24 hr. In contrast, the cells derived from the systemic vasculature showed a maximal induction of NOS transcript at 3 hr, and the level decreased from this time point to 24 hr. The full induct...","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"7 1","pages":"99-112"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88823298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1996-01-01DOI: 10.3109/10623329609024706
S. P. Spencer, P. Milner, P. Bodin, G. Burnstock
Human umbilical vessels are remarkable in lacking innervation; thus the role of the vascular endothelium is likely to be of prime importance in the local control of vascular tone. The vasoactive mediators arginine vasopressin (AVP), neuropeptide Y (NPY), vasoactive intestinal polypeptide (VIP), calcitonin gene-related peptide (CGRP) and substance P (SP) have been localised in the endothelial cells of human umbilical vessels but as yet no physiological roles have been assigned to their presence in this vessel. The effect of these vasoactive substances on the basal and thrombin-stimulated (10U/ml) release of the potent vasoconstrictor peptide endothelin-1 (ET-1) from cultured human umbilical vein endothelial cells was studied using an enzyme-linked immunosorbent assay. AVP (10−5 - 10−7M) increased basal and thrombin-stimulated ET-1 release. NPY (10dM) increased basal ET-1 release but did not significantly alter thrombin stimulated release. VIP (10−6 - 10−7M) exerted no significant effect on ET-1 release. CG...
{"title":"Modulation of Endothelin Release by Vasoactive Peptides Localised in Human Umbilical Vein Endothelial Cells","authors":"S. P. Spencer, P. Milner, P. Bodin, G. Burnstock","doi":"10.3109/10623329609024706","DOIUrl":"https://doi.org/10.3109/10623329609024706","url":null,"abstract":"Human umbilical vessels are remarkable in lacking innervation; thus the role of the vascular endothelium is likely to be of prime importance in the local control of vascular tone. The vasoactive mediators arginine vasopressin (AVP), neuropeptide Y (NPY), vasoactive intestinal polypeptide (VIP), calcitonin gene-related peptide (CGRP) and substance P (SP) have been localised in the endothelial cells of human umbilical vessels but as yet no physiological roles have been assigned to their presence in this vessel. The effect of these vasoactive substances on the basal and thrombin-stimulated (10U/ml) release of the potent vasoconstrictor peptide endothelin-1 (ET-1) from cultured human umbilical vein endothelial cells was studied using an enzyme-linked immunosorbent assay. AVP (10−5 - 10−7M) increased basal and thrombin-stimulated ET-1 release. NPY (10dM) increased basal ET-1 release but did not significantly alter thrombin stimulated release. VIP (10−6 - 10−7M) exerted no significant effect on ET-1 release. CG...","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"17 1","pages":"309-317"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82448045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1996-01-01DOI: 10.3109/10623329609024700
V. Latrille, O. Ghiringhelli, D. Jourdheuil-Rahmani, A. Barlatier, H. Bodard, P. Charpiot, J. Guillou, R. Luccioni, D. Garçon, P. Rolland
Vascular smooth muscle cells (VSMCs) activation and hyperplasia, the important etiologic factors in atherosclerosis development, are inhibitable by drugs which donate nitric oxide (NO). We tested the hypothesis that administration of ISDN (60 mg/day), a NO donor, would inhibit development of vascular hyperplasia in atherosclerotic minipigs. VSMC proliferation and NO release by endothelial cells (ECs) were investigated in freshly isolated cells from minipigs fed an atherogenic diet with oral ISDN treatment (n = 8) or without (n = 8), or a control diet (n = 8) for 4 months. In ECs, atherosclerosis depressed by 60% NO release and suppressed the L-arginine negative regulatory feedback of the NO-synthase. Concomitantly, a 4-fold increased proliferation (PCNA labelling) and a 2.3-fold activation (PDGF-BB labelling) were observed in atherosclerotic VSMCs. Long-term treatment of atherosclerotic animals with ISDN restored NO release and regulatory processes of NO synthase from ECs, and reduced by half the prolifer...
{"title":"Long-Term Treatment of Atherosclerotic Minipigs with Isosorbide Dinitrate Restores Nitric Oxide Release from Endothelial Cells, and Inhibits Vascular Smooth Muscle Cell Proliferation","authors":"V. Latrille, O. Ghiringhelli, D. Jourdheuil-Rahmani, A. Barlatier, H. Bodard, P. Charpiot, J. Guillou, R. Luccioni, D. Garçon, P. Rolland","doi":"10.3109/10623329609024700","DOIUrl":"https://doi.org/10.3109/10623329609024700","url":null,"abstract":"Vascular smooth muscle cells (VSMCs) activation and hyperplasia, the important etiologic factors in atherosclerosis development, are inhibitable by drugs which donate nitric oxide (NO). We tested the hypothesis that administration of ISDN (60 mg/day), a NO donor, would inhibit development of vascular hyperplasia in atherosclerotic minipigs. VSMC proliferation and NO release by endothelial cells (ECs) were investigated in freshly isolated cells from minipigs fed an atherogenic diet with oral ISDN treatment (n = 8) or without (n = 8), or a control diet (n = 8) for 4 months. In ECs, atherosclerosis depressed by 60% NO release and suppressed the L-arginine negative regulatory feedback of the NO-synthase. Concomitantly, a 4-fold increased proliferation (PCNA labelling) and a 2.3-fold activation (PDGF-BB labelling) were observed in atherosclerotic VSMCs. Long-term treatment of atherosclerotic animals with ISDN restored NO release and regulatory processes of NO synthase from ECs, and reduced by half the prolifer...","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"110 1","pages":"235-245"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75319174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1996-01-01DOI: 10.3109/10623329609024699
M. Dashwood, M. Timm, J. Kaski, Andrew J. Murdayz, B. Madden
In vitro autoradiographic studies, using sections of human epicardial coronary arteries, have demonstrated dense [125I]-endothelin-l binding to the tunica media and regions of the adventitia. Micro-autoradiography has been employed to localise binding at the cellular level and immunohistochemistry has been used to identify specific cell types on adjacent tissue sections. Adventitial [125I]-ET-1 binding is predominantly to microvessels, including those supplying the perivascular nerves. This binding is markedly reduced in the presence of unlabelled ET-1 and the ETA/ETB receptor antagonist bosentan. These results suggest that, apart from acting on vascular smooth muscle of the tunica media, the action of locally-released ET-1 may also be via adventitial microvessels, including those supplying the perivascular nerves.
{"title":"[125I]-ET=1 Binding to Perivascular Nerves of Human Epicardial Coronary Arteries","authors":"M. Dashwood, M. Timm, J. Kaski, Andrew J. Murdayz, B. Madden","doi":"10.3109/10623329609024699","DOIUrl":"https://doi.org/10.3109/10623329609024699","url":null,"abstract":"In vitro autoradiographic studies, using sections of human epicardial coronary arteries, have demonstrated dense [125I]-endothelin-l binding to the tunica media and regions of the adventitia. Micro-autoradiography has been employed to localise binding at the cellular level and immunohistochemistry has been used to identify specific cell types on adjacent tissue sections. Adventitial [125I]-ET-1 binding is predominantly to microvessels, including those supplying the perivascular nerves. This binding is markedly reduced in the presence of unlabelled ET-1 and the ETA/ETB receptor antagonist bosentan. These results suggest that, apart from acting on vascular smooth muscle of the tunica media, the action of locally-released ET-1 may also be via adventitial microvessels, including those supplying the perivascular nerves.","PeriodicalId":11588,"journal":{"name":"Endothelium-journal of Endothelial Cell Research","volume":"63 1","pages":"231-234"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80651522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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