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Vascular Pharmacology

Christoph H Saely, Heinz Drexel
Proprotein Convertase Subtilisin / Kexin 9 (PCSK9) plays an important role in the regulation of blood cholesterol levels, and inhibition of PCSK9 with monoclonal antibodies reduces LDL cholesterol by >50% over and above what can be achieved with statins or ezetimibe alone. Diet and exercise influence PCSK9 levels; however data on this issue are scarce. Regarding diet, a high oleic canola/docosahexaenoic acid oil blend, marine n-3 polyunsaturated fatty acids, vegetable n-6 polyunsaturated fatty acids, a Mediterranean style diet and acute fasting, but not necessarily weight reduction are associated with low PCSK9 concentrations, whereas a high fructose diet is associated with high PCSK9 concentrations...
October 13, 2016: Vascular Pharmacology
Jozef Dulak, M Yvonne Alexander, Anna M Randi
No abstract text is available yet for this article.
October 13, 2016: Vascular Pharmacology
Rosalinda Madonna, Raffaele De Caterina, Yong-Jian Geng
Characterized by progressive elevation of mean pulmonary artery pressure and pulmonary vascular resistance, pulmonary arterial hypertension (PAH) is an important health problem that contributes to right heart failure. Pulmonary arterial remodeling and constriction are two prominent features of PAH. It is a traditional view that increasing pulmonary blood flow and pressure, aerobic exercise does more harm than good to the pulmonary vasculature in PAH. However, recent studies have documented a potential benefit of low-intensity aerobic exercise for PAH patients...
October 5, 2016: Vascular Pharmacology
Po-Min Yang, Yu-Ting Huang, Yu-Qi Zhang, Chia-Wen Hsieh, Being-Sun Wung
The production of nitric oxide (NO) by endothelial NO synthase (eNOS) plays a major role in maintaining vascular homeostasis. This study elucidated the potential role of carbon monoxide (CO)-releasing molecules (CORMs) in NO production and explored the underlying mechanisms in endothelial cells. We observed that 25μM CORM-2 could increase NO production and stimulate an increase in the intracellular Ca(2+) level. Furthermore, ethylene glycol-bis(β-aminoethyl ether)-N,N,N',N'-tetra acetic acid caused CORM-2-induced NO production, which was abolished by 1,2-bis(2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid tetraacetoxy-methyl ester (BAPTA-AM), indicating that intracellular Ca(2+) release plays a major role in eNOS activation...
October 5, 2016: Vascular Pharmacology
Zuzanna Drebert, Mark MacAskill, Dahlia Doughty-Shenton, Karolien De Bosscher, Marc Bracke, Patrick W F Hadoke, Ilse M Beck
Angiogenesis is important in cancer progression and can be influenced by tumor-associated myofibroblasts. We addressed the hypothesis that glucocorticoids indirectly affect angiogenesis by altering the release of pro-angiogenic factors from colon cancer-derived myofibroblasts. Our study shows that glucocorticoids reduced prostanoids, urokinase-type plasminogen activator (uPA) and angiopoietin-like protein-2 (ANGPTL2) levels, but increased angiogenin (ANG) in supernatant from human CT5.3hTERT colon cancer-derived myofibroblasts...
October 4, 2016: Vascular Pharmacology
Weerapon Sangartit, Poungrat Pakdeechote, Veerapol Kukongviriyapan, Wanida Donpunha, Shigeki Shibahara, Upa Kukongviriyapan
Excessive iron can generate reactive oxygen species (ROS), leading to oxidative stress that is closely associated with cardiovascular dysfunction. Iron overload was induced in male ICR mice by injection of iron sucrose (10mg/kg/day) for eight weeks. Iron overload was evidenced by increased serum iron indices. The mice developed increased blood pressure, impaired vascular function and blunted response of the autonomic nervous system. These effects were accompanied by increased malondialdehyde levels in various tissues, increased nitric oxide metabolites in plasma and urine, and decreased blood glutathione...
October 3, 2016: Vascular Pharmacology
Yun-Yun He, Chun-Lei Liu, Xin Li, Rui-Jun Li, Li-Li Wang, Kun-Lun He
The phosphorylation of eukaryotic translation initiation factor 2 alpha (p-eIF2α) is essential for cell survival during hypoxia. The aim of this study was to investigate whether salubrinal, an inhibitor of p-eIF2α dephosphorylation could attenuate pulmonary arterial hypertension (PAH) and right ventricular (RV) hypertrophy in rats exposed to hypobaric hypoxia. PAH of rats was induced by hypobaric hypoxia. Salubrinal supplemented was randomized in either a prevention or a reversal protocol. At the end of the follow-up point, we measured echocardiography, hemodynamics, hematoxylin-eosin and Masson's trichrome stainings...
September 24, 2016: Vascular Pharmacology
Theiler Anna, Konya Viktoria, Pasterk Lisa, Maric Jovana, Bärnthaler Thomas, Lanz Ilse, Platzer Wolfgang, Schuligoi Rufina, Heinemann Akos
Endothelial dysfunction is a hallmark of inflammatory conditions. We recently demonstrated that prostaglandin (PG)E2 enhances the resistance of pulmonary endothelium in vitro and counteracts lipopolysaccharide (LPS)-induced pulmonary inflammation in vivo via EP4 receptors. The aim of this study was to investigate the role of the EP1/EP3 receptor agonist 17-phenyl-trinor-(pt)-PGE2 on acute lung inflammation in a mouse model. In LPS-induced pulmonary inflammation in mice, 17-pt.-PGE2 reduced neutrophil infiltration and inhibited vascular leakage...
September 21, 2016: Vascular Pharmacology
Anand M Prasad, Pimonrat Ketsawatsomkron, Daniel W Nuno, Olha M Koval, Megan E Dibbern, Ashlee N Venema, Curt D Sigmund, Kathryn G Lamping, Isabella M Grumbach
Angiotensin-II (Ang-II) is a well-established mediator of vascular remodeling. The multifunctional calcium-calmodulin-dependent kinase II (CaMKII) is activated by Ang-II and regulates Erk1/2 and Akt-dependent signaling in cultured smooth muscle cells in vitro. Its role in Ang-II-dependent vascular remodeling in vivo is far less defined. Using a model of transgenic CaMKII inhibition selectively in smooth muscle cells, we found that CaMKII inhibition exaggerated remodeling after chronic Ang-II treatment and agonist-dependent vasoconstriction in second-order mesenteric arteries...
September 20, 2016: Vascular Pharmacology
Masaharu Hazawa, Takeshi Yasuda, Ai Saotome-Nakamura, Kenichi Tomiyama, Chizuka Obara, Takaya Goto, Katsushi Tajima
Plasminogen activator inhibitor-1 (PAI-1) is induced by radiation resulting in endothelial cell impairment, potentially leading to multiple organ failure. Vitronectin (VN) is a 75-kDa glycoprotein (VN75) cleaved into two forms (VN75 or VN65/10) by furin, which is regulated by intracellular PAI-1. VN protects against radiation-induced endothelial cell death, but the mechanisms involved in VN processing and its interactions with intra- and extracellular PAI-1 remain unclear. We examined these processes in cells in vitro using recombinant proteins or overexpression of VN and PAI-1 genes, including furin-susceptible (T(381)) and furin-resistant VN (A(381))...
September 17, 2016: Vascular Pharmacology
Estella Zuccolo, Silvia Dragoni, Valentina Poletto, Paolo Catarsi, Daniele Guido, Alessandra Rappa, Marta Reforgiato, Francesco Lodola, Dmitry Lim, Vittorio Rosti, Germano Guerra, Francesco Moccia
Arachidonic acid (AA) stimulates endothelial cell (EC) proliferation through an increase in intracellular Ca(2+) concentration ([Ca(2+)]i), that, in turn, promotes nitric oxide (NO) release. AA-evoked Ca(2+) signals are mainly mediated by Transient Receptor Potential Vanilloid 4 (TRPV4) channels. Circulating endothelial colony forming cells (ECFCs) represent the only established precursors of ECs. In the present study, we therefore, sought to elucidate whether AA promotes human ECFC (hECFC) proliferation through an increase in [Ca(2+)]i and the following activation of the endothelial NO synthase (eNOS)...
September 12, 2016: Vascular Pharmacology
Agnieszka Jazwa, Urszula Florczyk, Anna Grochot-Przeczek, Bart Krist, Agnieszka Loboda, Alicja Jozkowicz, Jozef Dulak
Vascular endothelial growth factor (VEGF), as an endothelial cell-specific mitogen, is crucial for new blood vessels formation. Atherosclerosis affecting the cardiovascular system causes ischemia and functio laesa in tissues supplied by the occluded vessels. When such a situation occurs in the lower extremities, it causes critical limb ischemia (CLI) often requiring leg amputation. Low oxygen tension leads to upregulation of hypoxia-regulated genes (i.e. VEGF), that should help to restore the impaired blood flow...
September 9, 2016: Vascular Pharmacology
E Montaudon, L Dubreil, V Lalanne, B Jagu, G Toumaniantz, C Thorin, D Henrion, J-C Desfontis, L Martignat, M Y Mallem
OBJECTIVE: To evaluate whether active immunization producing β1- or β3-antibodies (β1-ABs and β3-ABs) detected in sera of patients with dilated cardiomyopathies has deleterious effects on vascular reactivity in Lewis rats thoracic aorta (TA) and small mesenteric arteries (SMA). DESIGN AND METHOD: Lewis rats were immunized for 6months with peptidic sequences corresponding to the second extracellular loop of β1- and β3-adrenoceptors (ARs). During the immunization, systolic blood pressure (SBP) was monitored using the tail cuff method...
September 9, 2016: Vascular Pharmacology
Cristina Zaragozá Arnaéz, Jorge Monserrat Sanz, Carolina Mantecón Ramiro, Lucinda Villaescusa Castillo, Francisco Zaragozá García, Melchor Álvarez de Mon Soto
Polyphenols are used as phlebotonic drugs, but their mechanism of action remains unknown. Since platelet activity and platelet-endothelial cell interactions are involved in the pathogenesis of cardiovascular disease, this work examines whether different flavonoid and coumarin drugs are able to inhibit platelet aggregation. This specific case of coumarins, the antiplatelet effect is not linked with a possible interaction over blood coagulation since this effect only dicoumarols have it. The antiplatelet capacity of polyphenols was assayed using peripheral blood platelets from healthy controls...
September 8, 2016: Vascular Pharmacology
Jie Li, Xiao-Yong Geng, Xiao-Liang Cong
No abstract text is available yet for this article.
September 8, 2016: Vascular Pharmacology
Rajesh G Mishra, Tzu-Ling Tseng, Mei-Fang Chen, Po-Yi Chen, Tony J-F Lee
Nitric oxide (NO) overproduction via induction of inducible nitric oxide synthase (iNOS) is implicated in vasodilatory shock in sepsis, leading to septic encephalopathy and accelerating cerebral ischemic injury. An abbreviated urea-cycle (L-citrulline-L-arginine-NO cycle) has been demonstrated in cerebral perivascular nitrergic nerves and endothelial cells but not in normal cerebral vascular smooth muscle cell (CVSMC). This cycle indicates that argininosuccinate synthase (ASS) catalyzes L-citrulline (L-cit) conversion to form argininosuccinate (AS), and subsequent AS cleavage by argininosuccinate lyase (ASL) forms L-arginine (L-arg), the substrate for NO synthesis...
September 7, 2016: Vascular Pharmacology
Carolin Zwadlo, Jürgen Borlak
Calcium channel blockers (CCB) differ in their effects on the cardiovascular system with diltiazem being less negatively ionotrop as compared to verapamil. Diltiazem is mainly used to treat supraventricular tachycardia, vasospastic angina and the Raynaud's syndrome. Little is known about the molecular effects of benzothiazepins on cardiac gene expression. We therefore investigated the effects of diltiazem on cardiac gene expression in normotensive and hypertensive rats with left ventricular hypertrophy and compared the results with our previous findings on verapamil and nifedipine...
September 6, 2016: Vascular Pharmacology
Yulong Chen, Hongmei Zhang, Enqi Liu, Cang-Bao Xu, Yaping Zhang
Vascular smooth muscle endothelin type B (ETB) receptor is involved in the pathogenesis of cardiovascular diseases (CVDs). Hyperhomocysteinemia is an independent risk factor for CVDs. The present study was designed to examine the hypothesis that homocysteine (Hcy) up-regulates vascular smooth muscle ETB receptors. In vitro experiments were performed in rat superior mesenteric artery (SMA) and vascular smooth muscle cells (VSMCs). The rat SMA or VSMCs were cultured in serum-free medium for 24h in the presence and absence of Hcy with or without specific inhibitors for the ERK1/2 signaling pathway and NF-κB...
August 31, 2016: Vascular Pharmacology
Peng Chu, Guozhu Han, Anil Ahsan, Zhengwu Sun, Shumin Liu, Zonghui Zhang, Bin Sun, Yanlin Song, Yuan Lin, Jinyong Peng, Zeyao Tang
Methylglyoxal (MGO), an active metabolite of glucose, can cause cellular injury which has an affinity for the progression of diabetes-associated atherosclerosis. Phosphocreatine (PCr) is a well-known high-energy phosphate compound. However, its protective effects and mechanism in the formation of a diabetes-associated atherosclerosis have not been clarified. In the present study, we investigated whether PCr could prevent MGO-induced apoptosis in human umbilical vascular endothelial cells (HUVECs) and explored the possible mechanisms...
August 30, 2016: Vascular Pharmacology
Agostino Virdis, Marco Gesi, Stefano Taddei
Reactive oxygen species (ROS) are generated by cell metabolism of oxygen and represent signaling molecules playing an active role in vascular biology. In pathological conditions, including hypertension, a ROS excess, together with reduced endogenous antioxidant defenses, occurs, determining a state of oxidative stress. NAD(P)H oxidase (Nox) is a major ROS source within the vasculature. A large body of literature has demonstrated that hypertension-associated vascular functional and structural changes are attributable to Nox-driven intravascular ROS generation...
August 25, 2016: Vascular Pharmacology
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