Dissertations / Theses on the topic 'Arterial Smooth Muscle Cell'
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Arshad, Haroon. "Mathematical modelling of pulmonary arterial smooth muscle cell subtypes." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/mathematical-modelling-of-pulmonaryarterial-smooth-muscle-cell-subtypes(c1110807-d94d-487c-90b8-8714d5e42d16).html.
Full textBeattie, David Keith. "The influence of altered haemodynamics on human smooth muscle cell behaviour." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.369122.
Full textHartley, S. A. "ATP regulated ion channels in arterial smooth muscle cells." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298264.
Full textCuringa, Gabrielle Mercedes. "The role of runt-related transcription factor 2 in arterial smooth muscle cell mineralization /." Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/6353.
Full textIzzard, Tanya. "Extracellular matrix and the cell cycle in vascular smooth muscle cells." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322616.
Full textSuttie, Andrew William. "Allylamine toxicity and dedifferentiation of arterial smooth muscle cells in vitro." Thesis, Queen Mary, University of London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.390596.
Full textProudfoot, Diane. "Effects of macrophage factors on the growth of arterial smooth muscle cells." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321094.
Full textWahl, Joel. "Development of Methods to Investigate Pulmonary Arterial Smooth Muscle Cells under Hypoxia." Licentiate thesis, Luleå tekniska universitet, Strömningslära och experimentell mekanik, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:ltu:diva-77140.
Full textWinter, Polly. "Endothelial and smooth muscle cell-to-cell communication within rat small mesenteric arteries." Thesis, University of Bath, 2007. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.436804.
Full textMyllärniemi, Marjukka. "Regulation of arterial smooth muscle cell proliferation after endothelial injury : an experimental approach to restenosis and transplant arteriosclerosis." Helsinki : University of Helsinki, 1999. http://ethesis.helsinki.fi/julkaisut/laa/trans/vk/myllarniemi/.
Full textPannu, Parveer Singh. "Regulation of ATP-binding cassette transporter A1 In intimal-type arterial smooth muscle cells." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/44171.
Full textDawson, Sarah Helen. "Identification and characterisation of a putative osteoprotegerin receptor on pulmonary arterial smooth muscle cells." Thesis, University of Sheffield, 2014. http://etheses.whiterose.ac.uk/9029/.
Full textPatel, J. "Smooth muscle cell proliferation and endothelin pathway in pulmonary arterial hypertension : comparative effects of current and putative therapeutic agents." Thesis, University College London (University of London), 2013. http://discovery.ucl.ac.uk/1400121/.
Full textCharolidi, Nicoletta. "Gap junctions in arterial smooth muscle cells : relationship between Connexin43 expression, intercellular communication and phenotype." Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501473.
Full textVan, Den Diepstraten Caroline H. "Analysis of apolipoprotein(a) fragments on proliferation and migration of human arterial smooth muscle cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0017/MQ52958.pdf.
Full textShaikh, Mohsin Ahmed. "Models of coupled smooth muscleand endothelial cells." Thesis, University of Canterbury. Centre for Bioengineering, 2011. http://hdl.handle.net/10092/6190.
Full textMcKean, Jenny Susan. "The role of the cAMP mediator Epac in vascular smooth muscle cell migration." Thesis, University of Aberdeen, 2015. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=227109.
Full textSu, Enming Joseph. "Role of angiotensin II in regulating smooth muscle cell replication in the vessel wall /." Thesis, Connect to this title online; UW restricted, 1998. http://hdl.handle.net/1773/6349.
Full textStickel, Diana [Verfasser], and Alexander [Akademischer Betreuer] Dietrich. "Cytosolic and mitochondrial Ca2+ handling in pulmonary arterial smooth muscle and endothelial cells / Diana Stickel ; Betreuer: Alexander Dietrich." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2017. http://d-nb.info/1127527908/34.
Full textKiskin, Fedir. "Developing an induced pluripotent stem cell model of pulmonary arterial hypertension to understand the contribution of BMPR2 mutations to disease-associated phenotypes in smooth muscle cells." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/285324.
Full textZhao, Jun, and e52677@ems rmit edu au. "The functional study of Na+/Ca2+ exchanger in vascular smooth muscle cells." RMIT University. Medical Sciences, 2007. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20080617.163746.
Full textHassan, Dhiya. "Forced Overexpression of Translationally Controlled Tumor Protein (TCTP/TPT1) Induces a Growth-Dysregulated Phenotype in Endothelial and Smooth Muscle Cells: Role of TCTP Exosomal Export in Paracrine Cell-Cell Signaling Induced by Endothelial Injury." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/38674.
Full textSimic, Damir. "Disclosure of novel mechanisms in which nicotine triggers structural and functional alterations of arterial smooth muscle cells, implications to pathogenesis of the occlusive arterial diseases." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ63106.pdf.
Full textTharp, Darla L. "Role of the intermediate-conductance Ca²⁺-activated K⁺ channel (K[ca]3.1) in coronary smooth muscle cell phenotypic modulation." Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/5936.
Full textThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Vita. "December 2007" Includes bibliographical references.
Holland, Michael. "A patch clamp study of pharmacological and physiological regulators of large conductance calcium-activated potassium channels in arterial smooth muscle cells." Thesis, University of Leicester, 1997. http://hdl.handle.net/2381/29937.
Full textLai, Ying-Ju [Verfasser]. "The Prostanoid EP4 receptor in prostacyclin sensing by pulmonary arterial smooth muscle cells in Monocrotaline-induced pulmonary hypertension in rats / Ying-Ju Lai." Gießen : Universitätsbibliothek, 2009. http://d-nb.info/1060450615/34.
Full textSmith, Andrew Hart. "THE ROLE OF CANONICAL TRANSIENT RECEPTOR POTENTIAL CHANNEL SUBTYPE-6 IN PHENOTYPIC MODULATION OF VASCULAR SMOOTH MUSCLE CELLS AND ARTERIAL HEALING AFTER VASCULAR INTERVENTION." Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case160710077734737.
Full textSeifert, Elena. "Metabolic Changes in Pulmonary Arterial Smooth Muscle Cells Exposed to Increased Mechanical Forces from an Ovine Model of Congenital Heart Disease with Increased Pulmonary Blood Flow." Scholarship @ Claremont, 2019. https://scholarship.claremont.edu/cmc_theses/2094.
Full textSharmin, Nahid. "Therapeutic Targeting of BMP and TGF-β Signalling Pathways for the Resolution of Pulmonary Arterial Hypertension." Thesis, University of Bradford, 2018. http://hdl.handle.net/10454/17177.
Full textCommonwealth Scholarship Commission in the UK
The full text will be available at the end of the embargo period, 31st July 2024.
Quatredeniers, Marceau. "Dérégulation du récepteur NMDA dans l'hypertension artérielle pulmonaire : conséquences et perspectives." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS574.
Full textPulmonary arterial hypertension (PAH) is a rare disease defined by an increase in mean pulmonary arterial pressure due to progressive obstruction of the small pulmonary arteries, leading to right heart failure and death. The vascular remodeling is a consequence of complex and multiple patho-mechanisms, including endothelial cells dysfunction and hyperproliferation of smooth muscle cells in the pulmonary vascular wall. The N-methyl-D-aspartate receptor (NMDAR), a glutamate receptor, has been recently identified as playing an active role in this vascular remodeling. It has been shown that in pulmonary arteries of PAH patients, NMDAR is overexpressed and overactivated and is involved in the proliferation and resistance to apoptosis of pulmonary vascular cells. However, the NMDAR subtype involved in this process remains unknown. The development of potential treatments targeting the NMDAR requires a better understanding of its subunit involvement in the disease. Since the GluN2A subunit is involved in the survival of neurons and the GluN2B subunit in their death, we hypothesized that the pulmonary vascular NMDAR subunit composition could be dysregulated in PAH. Therefore, in this thesis study we aimed to: i) study the composition of NMDAR in PAH, ii) explore its functional consequences in the pathophysiology of PAH, and iii) uncover its integration in the pathophysiology of PAH.We showed that the expression of the GluN2B subunit is reduced in the pulmonary arteries of PAH patients compared to non-PAH subjects. This occurs despite the overall increased expression of the obligatory GluN1 subunit, suggesting a switch from GluN2B-type receptors to, at least, another GluN2-type receptor. We also showed that in the presence of PDGF-BB, there is an immediate increase in the levels of phosphorylated Src family kinases (SFKs), associated to an increase in phosphorylated GluN2B (the active form) that were relocated to the cell membrane, suggesting the cross-talk between PDGF, SFKs and NMDAR. To validate the pathway, we inhibited the activation of PDGFR-β or SFKs, and in both cases the phosphorylation of GluN2B after PDGF stimulation was aborted. To assess the functional importance of this pathway, proliferation and “wound healing” tests were performed. The results clearly showed that selective inhibition of GluN2B, in the presence of PDGF, significantly increased both migration and proliferation of PASMCs. These results suggest that the lack of GluN2B-type receptors in PAH may potentiate SMC proliferative and migratory response to PDGF, a well-known overactivated pathway in PAH. In addition, we showed that GluN2A-type NMDARs arerecruited to the SMC membrane following PDGF stimulation, but the precise role of GluN2A-type NMDARs in PAH remains elusive. To further explore the crosstalk between the NMDAR and the PDGF receptor (PDGFR) pathways, we conducted a complementary bioinformatics study. To provide a model of the NMDAR signaling pathways in PAH we constructed and connected comprehensive knowledge bases of the actors involved in PAH on one hand and the signaling pathways involving NMDAR within the central nervous system on the other hand. Within these networks the NMDAR was revealed as a central downstream effector of the hallmark signaling pathways of PAH, including that of PDGFR.These results indicate that the membrane expression of GluN2A-type and GluN2B-type receptors is dysregulated in PAH, presumably switching the PDGF-dependent glutamate response towards GluN2A-type receptors. The consequences of such imbalance are the increased proliferation and migration of pulmonary vascular SMCs. Moreover, the lack of GluN2B-type NMDARs is a new feature in the pathophysiology of PAH and in the understanding of peripheral NMDA receptors in general. Besides, the NMDAR seems to be a central effector in PAH, interacting with multiple hallmark pathways of the disease, suggesting new tracks to further understanding the pathophysiology of PAH
Régent, Alexis. "Étude du rôle des cellules musculaires lisses vasculaires (CMLV) et des anticorps anti-CMLV dans la pathogénie de l’artérite à cellules géantes (maladie de Horton)." Thesis, Paris 5, 2014. http://www.theses.fr/2014PA05S021/document.
Full textBackground : Giant cell arteritis (GCA) is a large vessel vasculitis and its diagnosis usually relies on the identification of an inflammatory infiltrate made of mononuclear cells and giant cells upon temporal artery biopsy. There is also a remodeling process in the arterial wall due to an excessive proliferation of vascular smooth muscle cells (VSMC) which can sometimes lead to arterial occlusion. Purpose: Identify auto-antibodies targeting either endothelial cells (EC) and/or VSMC during GCA and better understand the role of VSMC in the remodeling process. Methods : Auto-antibodies were detected by a 2-dimensionnal immunoblot and their target antigens were identified by mass spectrometry. Proteoms of umbilical artery, pulmonary artery and aorta VSMC were compared by 2 dimension differential in gel electrophoresis (2D-DIGE). In order to identify mechanisms involved in VSMC proliferation in GCA, we used both 2D-DIGE and pan genomic chips in order to compare VSMC isolated at the time of temporal artery biopsy (TAB) from patients with a final diagnosis of GCA or another diagnosis. Results : In 15 patients with GCA, we identified lamin, vinculin and Annexin A5 as target antigens of anti-VSMC antibodies. Target antigens were linked with Grb2, an adaptator protein involved in VSMC proliferation. Normal VSMC originating from different vascular beds have differ in protein contents with differential expression of cytoskeleton and energy metabolism proteins. We compared VSMC from TAB with Ingenuity software and identified endothelin-1 (ET-1) and paxillin as proteins involved in vessel remodeling. We confirmed by immunohistichemistry and qPCR that ET-1 and its receptor ETAR and ETBR were expressed in temporal arteries from patients with GCA. Last, we reduced VSMC proliferation with Macitentan, an ETAR and ETBR antagonist and significantly inhibited VSMC proliferation with its active metabolite whereas other ET-1 inhibitors had no effect. Conclusion : We identified anti-VSMC auto-antibodies in patients with GCA. Their pathogenic role remains to be determined. Normal VSMC from different vascular locations differ in protein conten which might reflect different phenotypes and different properties. The escessive proliferation of VSMC from patients with GCA was inhibited by Macitentan. This drug might constitute a future therapeutic option
Wadsworth, R. M. "Regulation of contraction of arterial smooth muscle." Thesis, University of Strathclyde, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248764.
Full textBelozertseva, Ekaterina. "Effets du récepteur minéralocorticoïde, de l’intégrine αv et de vimentine sur les fonctions des cellules musculaires lisses vasculaires et la rigidité artérielle." Thesis, Université de Lorraine, 2016. http://www.theses.fr/2016LORR0165/document.
Full textArterial stiffness and fibrosis have a predictive value in the development of cardiovascular diseases (CV). These two phenotypes involve vascular smooth muscle cells (VSMCs) including membrane receptors and cytoskeletal proteins. The objectives were to examine: (i) the influence of the mineralocorticoid receptor (MR) on vascular reactivity, (ii) the role of avb3 integrin in the development of arterial stiffness and vascular fibrosis, and (iii) the impact of vimentin and synemin on arterial structure and function. The mice with genetic invalidation of the proteins of interest were used in these three studies. Results: the absence of MR decreased vascular reactivity by altering the contraction/relaxation coupling of VSMC through Ca2+- and NO-dependent mechanisms (a decrease of vasoconstriction in response to extracellular Ca2+ and impaired endothelium-dependent vasorelaxation in response to acetylcholine). The invalidation of the αv subunit prevented fibrosis in response to the administration of angiotensin II. The absence of vimentin, and not that of the synemin, increased arterial stiffness via changes in focal adhesions of VSMCs as well as endothelial cells. In conclusion, the studied membrane receptors and intracellular proteins that influenced the structure and function of arteries through specific actions on muscle tone, the mechanotransduction and the ultra-structural organization of VSMCs. These studies show the multifactorial dependency of the stiffness-fibrosis phenotypes of the arterial wall at the cellular and molecular levels. These results require more mechanistic work to determine the role of these proteins in CV diseases related to aging
Hautefort, Aurélie. "Etude des mécanismes inflammatoires, génétiques et épigénétiques impliqués dans la physiopathologie de l'hypertension artérielle pulmonaire." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS278.
Full textPulmonary arterial hypertension (PAH) is characterized by a progressive pulmonary arterial obstruction due to pulmonary vascular remodeling of distal arterioles as well as abnormal vasoconstriction. This project allowed to study three biological process clearly establish to be implicated in physiopathology of PAH.The first project demonstrated a dendritic cells dysfunction and a Th17 immune polarization of idiopathic PAH patients.The objective of the second project was to study the epigenetic variations in pulmonary endothelial cells (PEC) through a specific pattern of DNA methylation. We identified clusters of probes that discriminates controls and PAH patients. During bioinformatics study, ABCA1 (ATP binding cassette 1) gene was emphasized. Alteration of ABCA1 expression predicted during bioinformatics study has been validated in human and in monocrotaline rat model.The last project described the validation of a new PAH model by a hemodynamic, histological, vascular, molecular and electrophysiological characterization of heterozygous rat mutated to Bmpr2 gene. Whole functional and molecular dysregulation define this animal model like a useful tool in the study of BMPRII signaling alteration in PAH physiopathology
Goonetilleke, Lakshman. "Two-pore domain potassium channels in arterial smooth muscle." Thesis, University of Liverpool, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.485866.
Full textCosta, Edilene de Souza. "Efeito da proteína dissulfeto isomerase na ativação do receptor do fator de crescimento epidermal (EGFR) durante o desenvolvimento da hipertensão arterial. Papel da Nox1 NADPH oxidase." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-16082016-103430/.
Full textStudies characterizing the involvement of PDI in the modulation of ROS by Nox1 as modulators of cell migration of vascular smooth muscle (VSMC) mediated by growth factors derived from platelets (PDGF). Other studies have demonstrated the involvement of the epidermal growth factor receptor (EGFR) on vascular remodeling after transactivation via Angiotensin II. However the role of PDI in the activation of EGFR via Nox1 in hypertension remains unknown. Objective was to characterize the role of PDI in Nox1 dependent EGFR expression during the development of hypertension. Results show an increase of HB-EGF expression and ERK 1/2 activation in the aortic SHR at 8 weeks and 12 weeks of age, and plasma SHR at 12 weeks. Still, the OvxPDI resulted in an increase in gene expression of Nox-1 both in OVXPDI and in OvxPDIMUT way. Results show a new role of PDI in gene expression of Nox-1 via EGFR and the participation of this thiol reductase oxide in the pathogenesis of hypertension.
Schnetzer, Karen Joan. "Effects of in vitro uniaxial cyclic stretch upon rat aortic smooth muscle cells." Diss., Georgia Institute of Technology, 1995. http://hdl.handle.net/1853/10236.
Full textBrennan, Sean. "KV7 potassium channels : a focus on human intra-pulmonary arteries." Thesis, University of Manchester, 2015. https://www.research.manchester.ac.uk/portal/en/theses/kv7-potassium-channels-a-focus-on-human-intrapulmonary-arteries(46f5ff0e-1674-4ab1-916d-2f43e3c585e5).html.
Full textFellows, Adam Lee. "FOXO3a in vascular smooth muscle cell apoptosis." Thesis, University of Cambridge, 2018. https://www.repository.cam.ac.uk/handle/1810/275687.
Full textMcSherry, Iain Neil. "Endothelial cell modulation of smooth muscle contraction." Thesis, University of Bath, 2005. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.423481.
Full textRuiz, Matthieu. "Rôle de PGC-1α dans le système cardiovasculaire : recherche d’activateurs cœur-spécifiques et étude de ses mécanismes de régulation dans le muscle lisse aortique." Thesis, Paris 11, 2012. http://www.theses.fr/2012PA114830/document.
Full textHeart failure (HF) is still the major cause of morbimortality in industrialized countries that justify the research of new treatments. Characterized in part by metabolic disorders including mitochondrial dysfunction, energetic metabolism appears as an essential component in HF development. These last years, PGC-1α has been proposed as a central actor of mitochondrial function control and thus as a therapeutic target of interest.The development of a cellular robotized assay in cardiac-like differentiated H9c2 cells allowed identification of three families: steroid hormones, B vitamins and fatty acids, able to induce the expression of PGC-1α and thus up-regulate mitochondrial biogenesis and mitochondrial respiration. The validation of these effects in adult rat cardiomyocytes lets in the one hand to validate the suitability of the assay and in the other hand to confirm that PGC-1α induction leads to mitochondrial biogenesis activation. Consequently, this assay constitutes a major asset to find new activators of PGC-1α to better understand its regulation in heart and provides interesting perspectives for the research of therapeutic pharmacologic compounds.Mechanisms controlling mitochondrial biogenesis in response to hypertension in vascular smooth muscle remain unclear. In this context, the second part of this work was to identify how mitochondrial biogenesis is modulated in arterial hypertension. Using an experimental model of hypertension and after validation in cultivated smooth muscle cells, we show a mitochondrial biogenesis induction in response to hypertension in relation with an increase in oxidative stress. Moreover, this induction is associated with a significant increase in CaMKII activity which was totally blocked by an antioxidant: resveratrol. These results suggest a regulation of mitochondrial biogenesis by oxidative stress via a CaMKII mechanism in vascular smooth muscle
Brown-Turner, Dawn Leah. "Regulation of alpha- and beta-actin isoforms in the contracting A7r5 smooth muscle cell." [Huntington, WV : Marshall University Libraries], 2009. http://www.marshall.edu/etd/descript.asp?ref=1009.
Full textZhao, Ning. "Notch Signaling Guides Vascular Smooth Muscle Cell Function." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1396890017.
Full textKinnear, Nicholas Patrick. "An investigation on NAADP-dependent Ca²⁺ signalling mechanisms in arterial smooth muscle /." St Andrews, 2007. http://hdl.handle.net/10023/364.
Full textTurner, Joanne L. "Ionic currents in pulmonary arterial smooth muscle and the effect of hypoxia." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360012.
Full textKinnear, Nicholas P. "An investigation of NAADP-dependent Ca²⁺ signalling mechanisms in arterial smooth muscle." Thesis, University of St Andrews, 2007. http://hdl.handle.net/10023/364.
Full textChaudhry, Adil Anthony. "Transient postnatal pulmonary arterial smooth muscle cytoskeletal disassembly and its functional implications." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327049.
Full textJia, Yanlin. "Nitric oxide and airway smooth muscle responsiveness." Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=29052.
Full textNO is known to be synthesized from L-arginine in a reaction catalyzed by NO synthase (NOS). Liver cytochrome P450 also catalyzes the oxidative cleavage of C=N bonds of compounds containing a -C(NH$ sb2$)NOH function, producing NO in vitro. We hypothesized that the biosynthesis of NO in airway smooth muscle cells could result from P450 enzymes acting on appropriate substrates. NO can be synthesized in a number of lung cell types. However, to date, no constitutive form of NOS activity has been found in airway smooth muscle cells. We next examined the possibility that airway smooth muscle itself might be able to synthesize NO. Formamidoxime, a compound containing the -C(NH$ sb2$)NOH function, was found to produce NO in cultured airway smooth muscle cells. As well, formamidoxime relaxed pre-contracted trachealis and cyclic GMP accumulation in airway smooth muscle cells in culture. These effects were inhibited by P450 inhibitors but not by NOS inhibitors. Thus, an L-arginine-independent pathway for production of NO was demonstrable in airway smooth muscle cells. This NO production was catalyzed by P450 but not by NOS.
In conclusion, my studies have demonstrated an important role for endogenous NO production in determining the airway responsiveness of normal rats to inhaled cholinergic agonists. This mechanism contributes to strain-related differences in airway responsiveness in the rat.
Wong, Wai-ming. "Effects of isoflavonoids on vascular smooth muscle cell proliferation /." View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36433913.
Full textLin, Cho-Hao. "Endothelial cell-dependent Notch Signaling Regulates Vascular Smooth Muscle Cell Phenotypes." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1429269211.
Full text