Articles de revues : « VEGF, HYPERTENSION »

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Grover, Theresa R., Thomas A. Parker, Jeanne P. Zenge, Neil E. Markham, John P. Kinsella et Steven H. Abman. « Intrauterine hypertension decreases lung VEGF expression and VEGF inhibition causes pulmonary hypertension in the ovine fetus ». American Journal of Physiology-Lung Cellular and Molecular Physiology 284, n^o 3 (1 mars 2003) : L508—L517. http://dx.doi.org/10.1152/ajplung.00135.2002.

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Although vascular endothelial growth factor (VEGF) plays a vital role in lung vascular growth in the embryo, its role in maintaining endothelial function and modulating vascular structure during late fetal life has not been studied. We hypothesized that impaired lung VEGF signaling causes pulmonary hypertension, endothelial dysfunction, and structural remodeling before birth. To determine whether lung VEGF expression is decreased in an experimental model of persistent pulmonary hypertension of the newborn (PPHN), we measured lung VEGF and VEGF receptor protein content from fetal lambs 7–10 days after ductus arteriosus ligation (132–140 days gestation; term = 147 days). In contrast with the surge in lung VEGF expression during late gestation in controls, chronic intrauterine pulmonary hypertension reduced lung VEGF expression by 78%. To determine whether VEGF inhibition during late gestation causes pulmonary hypertension, we treated fetal lambs with EYE001, an aptamer that specifically inhibits VEGF165. Compared with vehicle controls, EYE001 treatment elevated pulmonary artery pressure and pulmonary vascular resistance by 22 and 50%, respectively, caused right ventricular hypertrophy, and increased wall thickness of small pulmonary arteries. EYE001 treatment reduced lung endothelial nitric oxide synthase protein content by 50% and preferentially impaired the pulmonary vasodilator response to ACh, an endothelium-dependent agent. We conclude that chronic intrauterine pulmonary hypertension markedly decreases lung VEGF expression and that selective inhibition of VEGF165 mimics the structural and physiological changes of experimental PPHN. We speculate that hypertension downregulates VEGF expression in the developing lung and that impaired VEGF signaling may contribute to the pathogenesis of PPHN.

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Marini, M., D. Vichi, A. Toscano, G. D. Zappoli Thyrion, E. Parretti, G. Mello, G. Gheri, A. Pacini et E. Sgambati. « Expression of vascular endothelial growth factor receptor types 1, 2 and 3 in placenta from pregnancies complicated by hypertensive disorders ». Reproduction, Fertility and Development 19, n^o 5 (2007) : 641. http://dx.doi.org/10.1071/rd06131.

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The aim of the present study was to determine the expression of vascular endothelial growth factor (VEGF) family receptors (VEGFR) in placentas from pregnancies complicated by hypertensive disorders of different clinical severity. Placental tissue from women with gestational hypertension, pre-eclampsia, pre-eclampsia with haemolysis, elevated liver enzymes and low platelets (HELLP syndrome) and normotensive women, as a control group, was examined. Immunohistochemical techniques, reverse transcription–polymerase chain reaction and western blot were used to evaluate receptor expression. In cases with gestational hypertension, as well as in control cases, VEGFR-1 and VEGFR-3 immunoreactivity was detected in all placental components, whereas in placentas from the pre-eclampsia and pre-eclampsia with HELLP syndrome groups, VEGFR-1 and VEGFR-3 immunoreactivity was detected only in some portions of trophoblast and/or some vessels and/or clusters of stromal cells. In the control group, VEGFR-2 immunoreactivity was observed only in the vessels, whereas the hypertensive groups showed VEGF-2 immunoreactivity also in trophoblast and stromal cells. The mRNA levels of the three receptors in the group with gestational hypertension were higher with respect to those in the control group. Placentas from pregnancies with pre-eclampsia showed lowest mRNA expression levels, whereas placentas from women with pre-eclampsia plus HELLP syndrome showed higher mRNA expression levels with respect to the three other groups. Receptor protein levels were lower in pathological cases compared with levles in the control group. These findings demonstrate a dysregulation of placental expression of VEGF family receptors related to the degree of clinical severity of the hypertensive disorder.

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Kobalava, Zh D., et E. K. Shavarova. « Hypertension related to the antitumor treatment with angiogenesis inhibitors : an iatrogenic hypertension ». "Arterial’naya Gipertenziya" ("Arterial Hypertension") 24, n^o 4 (26 septembre 2018) : 384–95. http://dx.doi.org/10.18705/1607-419x-2018-24-4-384-395.

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One of the key regulators of vascular tone is the vascular endothelial growth factor (VEGF), which can enhance the production of nitric oxide, a potent vasodilator, and reduce vascular resistance by generating new vessels. Both mechanisms contribute to blood pressure decrease. The implementation of a new class of antitumor therapy — inhibitors of VEGF signaling pathway — results in the growth of cardiovascular complications such as arterial hypertension (HTN). The paper analyzes the causes of HTN development, approaches to the timely diagnosis of HTN and the correct assessment of cardiovascular risk before administration of VEGF inhibitors and during the treatment. We also review the features of the approaches of elevated blood pressure management in patients receiving targeted therapy.

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Louzier, Vanessa, Bernadette Raffestin, Aude Leroux, Didier Branellec, Jean Michel Caillaud, Micheline Levame, Saadia Eddahibi et Serge Adnot. « Role of VEGF-B in the lung during development of chronic hypoxic pulmonary hypertension ». American Journal of Physiology-Lung Cellular and Molecular Physiology 284, n^o 6 (1 juin 2003) : L926—L937. http://dx.doi.org/10.1152/ajplung.00247.2002.

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Angiogenic factors exert protective effects on the lung. To investigate the effect of VEGF-B, a factor coexpressed in the lung with VEGF-A, we assessed chronic hypoxic pulmonary hypertension in VEGF-B knockout mice (VEGF-B−/−) and in rats with lung overexpression of VEGF-B induced by adenovirus transfer. No significant difference in pulmonary hemodynamics, right ventricular hypertrophy, distal vessel muscularization, or vascular density was found between VEGF-B−/− and control mice after 3 wk of hypoxia. When overexpressed, VEGF-B167 or VEGF-B186 had protective effects similar to those of human VEGF-A165. Lung endothelial nitric oxide synthase (eNOS) expression was increased by 5 days of hypoxia or VEGF-A adenovirus vector (Ad.VEGF-A) overexpression, whereas VEGF-B167 or VEGF-B186had no effect. With hypoxia or normoxia, the wet-to-dry lung weight ratio was increased 5 days after Ad.VEGF-A administration compared with control (Ad.nul), Ad.VEGF-B167, or Ad.VEGF-B186. Endogenous VEGF-B does not counteract the development of hypoxic pulmonary hypertension. However, when overexpressed in the lung, VEGF-B can be as potent as VEGF-A in attenuating pulmonary hypertension, although it has no effect on eNOS expression or vascular permeability.

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Bhargava, Pankaj. « VEGF kinase inhibitors : how do they cause hypertension ? » American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 297, n^o 1 (juillet 2009) : R1—R5. http://dx.doi.org/10.1152/ajpregu.90502.2008.

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Neoangiogenesis is a critical phenomenon enabling the growth and metastasis of tumors, and inhibitors of neoangiogenesis have been recently added to the armamentarium of anticancer therapies available for clinical use. Dysregulated signaling through the vascular endothelial growth factor (VEGF) pathway has been implicated as a key mediator of neoangiogenesis in tumors. Agents that block signaling through the VEGF pathway demonstrated tumor shrinkage in preclinical models and were therefore developed as anticancer therapies for use in humans. VEGF kinase inhibitors are being used in the treatment of a wide variety of cancers, and recent studies have shown that patients will likely require long-term treatment with these agents. Hypertension has emerged as a frequent side effect associated with agents that block signaling through the VEGF pathway. A thorough understanding of the mechanisms underlying hypertension is crucial to developing appropriate therapeutic strategies for treating hypertension associated with VEGF kinase inhibitors. Several recent studies have advanced our understanding of the pathophysiology of hypertension associated with VEGF kinase inhibitors and will be the subject of this review.

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Pearson, Roy Douglas. « Placental Malaria : Hypertension, VEGF, and Prolactin ». PLoS Medicine 4, n^o 3 (27 mars 2007) : e141. http://dx.doi.org/10.1371/journal.pmed.0040141.

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Hayman, Suzanne R., Nelson Leung, Joseph P. Grande et Vesna D. Garovic. « VEGF Inhibition, Hypertension, and Renal Toxicity ». Current Oncology Reports 14, n^o 4 (29 avril 2012) : 285–94. http://dx.doi.org/10.1007/s11912-012-0242-z.

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Newton, Herbert B. « Bevacizumab : Review of Development, Pharmacology, and Application to Brain Tumors ». Clinical Medicine. Therapeutics 1 (janvier 2009) : CMT.S2042. http://dx.doi.org/10.4137/cmt.s2042.

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Bevacizumab is a humanised monoclonal antibody targeted to the vascular endothelial growth factor (VEGF). VEGF is the ligand for VEGF receptors (VEGFR), which are important for the development and maintenance of the angiogenic phenotype in high-grade solid tumors, including malignant gliomas. An overview of angiogenesis, VEGF, VEGFR, and the pharmacology of bevacizumab will be presented. Bevacizumab is active in pre-clinical testing against glioma tissue cultures and xenograft models. In the clinical setting, in combination with irinotecan and other chemotherapy agents, it has shown significant activity in patients with glioblastoma multiforme (GBM) and other brain tumors. Objective responses on neuro-imaging have been noted in 30%-60% of reported cases. Prolongation of progression-free survival and overall survival have also been suggested in many reports. Treatment of bevacizumab is associated with potential side effects, including thromboembolic disorders, fatigue, intracranial hemorrhage, proteinuria, hypertension, and bowel perforation.

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Le Cras, Timothy D., Neil E. Markham, Rubin M. Tuder, Norbert F. Voelkel et Steven H. Abman. « Treatment of newborn rats with a VEGF receptor inhibitor causes pulmonary hypertension and abnormal lung structure ». American Journal of Physiology-Lung Cellular and Molecular Physiology 283, n^o 3 (1 septembre 2002) : L555—L562. http://dx.doi.org/10.1152/ajplung.00408.2001.

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To determine whether disruption of vascular endothelial growth factor (VEGF)-VEGF receptor (VEGFR) signaling in the newborn has long-term effects on lung structure and function, we injected 1-day-old newborn rat pups with a single dose of Su-5416, a VEGFR inhibitor, or vehicle (controls). Lungs from infant (3-wk-old) and adult (3- to 4-mo-old) rats treated with Su-5416 as newborns showed reductions in arterial density (82 and 31%, respectively) and alveolar counts (45 and 29%) compared with controls. Neonatal treatment with Su-5416 increased right ventricle weight to body wt ratios (4.2-fold and 2.0-fold) and pulmonary arterial wall thickness measurements (2.7-fold and 1.6-fold) in infant and adult rats, respectively, indicating marked pulmonary hypertension. We conclude that treatment of newborn rats with the VEGFR inhibitor Su-5416 impaired pulmonary vascular growth and postnatal alveolarization and caused pulmonary hypertension and that these effects were long term, persisting well into adulthood.

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Yang, Guo-Hong, Xin Zhou, Wen-Jie Ji, Shan Zeng, Yan Dong, Lu Tian, Ying Bi et al. « Overexpression of VEGF-C attenuates chronic high salt intake-induced left ventricular maladaptive remodeling in spontaneously hypertensive rats ». American Journal of Physiology-Heart and Circulatory Physiology 306, n^o 4 (15 février 2014) : H598—H609. http://dx.doi.org/10.1152/ajpheart.00585.2013.

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Recent studies have shown that the tonicity-responsive enhancer binding protein (TonEBP)/vascular endothelial growth factor-C (VEGF-C) signaling pathway-induced lymphangiogenesis provides a buffering mechanism for high salt (HS) intake-induced elevation of blood pressure (BP). Moreover, blocking of TonEBP/VEGF-C signaling by mononuclear phagocyte depletion can induce salt-sensitive hypertension in rats. We hypothesized that HS intake could have an impact on cardiac lymphangiogenesis, and regulation of VEGF-C bioactivity, which is largely through the main receptor for VEGFR-3, may modulate HS intake-induced left ventricular remodeling. We demonstrated upregulation of TonEBP, increased macrophage infiltration, and enhanced lymphangiogenesis in the left ventricles of spontaneously hypertensive rats (SHR) that were fed a HS diet (8.0% NaCl). Then, retrovirus vectors capable of overexpression (ΔNΔC/VEGF-C/Cys152Ser, used for overexpressing VEGF-C) and blocking (VEGFR-3-Rg, used for trapping of bioactive VEGF-C) of VEGF-C and control vector (pLPCX) were intravenously administered to SHR from week 9 of a 12-wk HS loading period. At the end of the HS challenge, overexpression of VEGF-C led to enhanced cardiac lymphangiogenesis, decreased myocardial fibrosis, and macrophage infiltration, preserved left ventricular functions, as well as decreased blood pressure level compared with the HS group and the control vector-treated HS group. In contrast, systemic blocking of VEGF-C was associated with elevation of blood pressure level and an exacerbation of hypertensive left ventricular remodeling, as indicated by increased fibrosis and macrophage infiltration, and diminished lymphangiogenesis. Hence, our findings highlight that VEGF-C/VEGFR-3 is a promising therapeutic target to attenuate hypertensive left ventricular remodeling induced by HS intake, presumably via blood pressure-dependent and -independent mechanisms.

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TSAI, Wei-Chuan, Yi-Heng LI, Yao-Yi HUANG, Chin-Chan LIN, Ting-Hsing CHAO et Jyh-Hong CHEN. « Plasma vascular endothelial growth factor as a marker for early vascular damage in hypertension ». Clinical Science 109, n^o 1 (23 juin 2005) : 39–43. http://dx.doi.org/10.1042/cs20040307.

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Elevation of plasma VEGF (vascular endothelial growth factor) has been noted in patients with hypertension or atherosclerosis. VEGF has been regarded as a marker for endothelial dysfunction. However, the role of VEGF in hypertension-induced vascular injury and its relationship with endothelial function have not been studied. This study included 20 untreated hypertensive men with grade 1 or 2 hypertensive retinopathy, 10 untreated hypertensive men without hypertensive retinopathy and 10 healthy controls. None of the hypertensive patients had diabetes, renal impairment or overt vascular diseases. Plasma VEGF and adhesion molecules were measured using ELISAs. Endothelial function was measured by FMD (flow-mediated vasodilation) of the brachial artery. Plasma levels of VEGF, excluding adhesion molecules, were significantly higher in hypertensive patients with retinopathy when compared with patients without retinopathy (152.4±80.8 pg/ml versus 104.7±27.2 pg/ml, P=0.035) or controls (152.4±80.8 pg/ml versus 98.9±23.7 pg/ml, P=0.025). Levels of FMD were significantly lower in hypertensive patients than controls, but there were no significant differences between patients with or without retinopathy. Degrees of FMD were inversely correlated with VEGF levels (r=−0.351, P=0.031). Elevation of plasma VEGF was associated with hypertensive retinopathy. Plasma VEGF could be used as a marker of early vascular damage induced by hypertension.

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Tang, Jen-Ruey, Gregory J. Seedorf, Vincent Muehlethaler, Deandra L. Walker, Neil E. Markham, Vivek Balasubramaniam et Steven H. Abman. « Moderate postnatal hyperoxia accelerates lung growth and attenuates pulmonary hypertension in infant rats after exposure to intra-amniotic endotoxin ». American Journal of Physiology-Lung Cellular and Molecular Physiology 299, n^o 6 (décembre 2010) : L735—L748. http://dx.doi.org/10.1152/ajplung.00153.2010.

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To determine the separate and interactive effects of fetal inflammation and neonatal hyperoxia on the developing lung, we hypothesized that: 1) antenatal endotoxin (ETX) causes sustained abnormalities of infant lung structure; and 2) postnatal hyperoxia augments the adverse effects of antenatal ETX on infant lung growth. Escherichia coli ETX or saline (SA) was injected into amniotic sacs in pregnant Sprague-Dawley rats at 20 days of gestation. Pups were delivered 2 days later and raised in room air (RA) or moderate hyperoxia (O2, 80% O2 at Denver's altitude, ∼65% O2 at sea level) from birth through 14 days of age. Heart and lung tissues were harvested for measurements. Intra-amniotic ETX caused right ventricular hypertrophy (RVH) and decreased lung vascular endothelial growth factor (VEGF) and VEGF receptor-2 (VEGFR-2) protein contents at birth. In ETX-exposed rats (ETX-RA), alveolarization and vessel density were decreased, pulmonary vascular wall thickness percentage was increased, and RVH was persistent throughout the study period compared with controls (SA-RA). After antenatal ETX, moderate hyperoxia increased lung VEGF and VEGFR-2 protein contents in ETX-O2 rats and improved their alveolar and vascular structure and RVH compared with ETX-RA rats. In contrast, severe hyperoxia (≥95% O2 at Denver's altitude) further reduced lung vessel density after intra-amniotic ETX exposure. We conclude that intra-amniotic ETX induces fetal pulmonary hypertension and causes persistent abnormalities of lung structure with sustained pulmonary hypertension in infant rats. Moreover, moderate postnatal hyperoxia after antenatal ETX restores lung growth and prevents pulmonary hypertension during infancy.

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Goodlett, Bethany L., Chang Sun Kang, Eunsoo Yoo, Shobana Navaneethabalakrishnan, Dakshnapriya Balasubbramanian, Sydney E. Love, Braden M. Sims et al. « A Kidney-Targeted Nanoparticle to Augment Renal Lymphatic Density Decreases Blood Pressure in Hypertensive Mice ». Pharmaceutics 14, n^o 1 (30 décembre 2021) : 84. http://dx.doi.org/10.3390/pharmaceutics14010084.

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Chronic interstitial inflammation and renal infiltration of activated immune cells play an integral role in hypertension. Lymphatics regulate inflammation through clearance of immune cells and excess interstitial fluid. Previously, we demonstrated increasing renal lymphangiogenesis prevents hypertension in mice. We hypothesized that targeted nanoparticle delivery of vascular endothelial growth factor-C (VEGF-C) to the kidney would induce renal lymphangiogenesis, lowering blood pressure in hypertensive mice. A kidney-targeting nanoparticle was loaded with a VEGF receptor-3-specific form of VEGF-C and injected into mice with angiotensin II-induced hypertension or LNAME-induced hypertension every 3 days. Nanoparticle-treated mice exhibited increased renal lymphatic vessel density and width compared to hypertensive mice injected with VEGF-C alone. Nanoparticle-treated mice exhibited decreased systolic blood pressure, decreased pro-inflammatory renal immune cells, and increased urinary fractional excretion of sodium. Our findings demonstrate that pharmacologically expanding renal lymphatics decreases blood pressure and is associated with favorable alterations in renal immune cells and increased sodium excretion.

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Katsi, Vasiliki, Zerdes Ioannis, Manolakou Stavroula, Makris Thomas, Nihoyannopoulos Petros, Tousoulis Dimitris et Kallikazaros Ioannis. « Anti-VEGF Anticancer Drugs : Mind the Hypertension ». Recent Advances in Cardiovascular Drug Discovery (Formerly Recent Patents on Cardiovascular Drug Discovery) 9, n^o 2 (30 juillet 2015) : 63–72. http://dx.doi.org/10.2174/1574890110999150604114127.

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Badri, Shirinsadat, Lillian Siberian, Rasool Soltani, Azadeh Moghaddas, Sara Ataei et Mahnaz Momenzadeh. « Nephrotoxicity induced by vascular endothelial growth factor inhibitors ». Journal of Nephropharmacology 11, n^o 1 (6 octobre 2021) : e4-e4. http://dx.doi.org/10.34172/npj.2022.04.

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Vascular endothelial growth factor (VEGF) is a special mitogen for vascular endothelial cells, an essential endogenous angiogenic cytokine, and the principal controller of vascular growth that plays a fundamental role in therapeutic angiogenesis pathways. VEGF-targeted therapy is categorized into the group of angiogenesis inhibitors that inhibit the expression or the activity of VEGF. It comprises counteracting VEGF antibodies, VEGF receptors, VEGF-trap, and tyrosine kinase inhibitor (TKIs) with selectivity for VEGF receptors. The kidney is both a target and a source of VEGF. VEGF may be a vital mediator to restore some types of renal diseases (e.g., non-diabetic renal diseases) and harmful in some other diseases (e.g., diabetes and diabetes complications). Due to their ability to prevent angiogenesis, VEGF inhibitors have been found as a powerful tool to treat angiogenesis-dependent diseases, including cancer and diabetic retinopathy. VEGF preserves the renal structure and function in normal physiologic conditions. Therefore, all treatments that inhibit the VEGF pathway may lead to renal disorders, especially renovascular diseases such as hypertension, proteinuria, nephrotic syndrome, decreased glomerular filtration rate (GFR), and thrombotic microangiopathy (TMA). In the present study, we reviewed some related reports and associated mechanisms, especially for hypertension and proteinuria.

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Grechukhina, Katerina S., Natalia V. Chebotareva et Tatyana N. Krasnova. « Nephrotoxicity of anti-angiogenesis drugs ». Terapevticheskii arkhiv 92, n^o 6 (9 juillet 2020) : 93–98. http://dx.doi.org/10.26442/00403660.2020.06.000672.

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Neoangiogenesis is a basic factor for most physiological as well as pathological processes i.e. tumor metastases. The most important is vascular endothelium growth factor (VEGF) and its receptors (VEGFR1/2) in angiogenesis processes. Nowadays antiangiogenic agents (which inhibit VEGF like bevacizumab neither VEGFR2 like ramucirumab) are widely used in very different chemotherapeutic regimens in clinical oncology. The signalling pathway VEGF-VEGFR plays a crucial role in supporting of adequate kidney function. Appearance of antiangiogenic drugs led to adverse nephrotoxic effects: arterial hypertension, proteinuria, rarely nephrotic syndrome, and kidney dysfunction. Various hystological variants of nephropathy are described, however, in most cases, signs of thrombotic microangiopathy of the renal vessels are noted. This literature review discusses mechanisms, clinical and morphological aspects of nephropathy associated with antiangiogenic drugs.

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Nadar, Sunil, Ioannis Karalis, Eman Al Yemeni, Andrew Blann et Gregory Lip. « Plasma markers of angiogenesis in pregnancy induced hypertension ». Thrombosis and Haemostasis 94, n^o 11 (2005) : 1071–76. http://dx.doi.org/10.1160/th05-03-0167.

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SummaryThis study tests the hypothesis that abnormalities in plasma indices of angiogenesis, such as Vascular Endothelial Growth Factor (VEGF) and angiopoietins (Ang-1, Ang-2), as well as their soluble receptors Flt-1 (sflt-1) and Tie 2 (sTie-2) respectively, are present in women with in pregnancy-induced hypertension (PIH). We also measured platelet levels of VEGF and Ang-1 (pVEGF and pAng-1 respectively). We studied 69 consecutive women with PIH (34 without proteinuria, and 35 with proteinuria, i.e. preeclampsia) who were compared to 64 consecutive women with normotensive pregnancies and 30 normotensive non-pregnant women, in a cross-sectional study. Using ELISA, we measured levels of plasma VEGF, Ang-1 &2, Tie-2 and sflt-1, and also the levels of angiogenic markers within the platelet [platelet VEGF (pVEGF) and platelet Ang-1 (pAng1)] by lysing a fixed number of platelets with 0.5% tween. Results show that levels of plasma VEGF, Ang-1, Ang2, sFlt-1 and Tie-2 were significantly different between the study groups. Post hoc analyses revealed plasma Ang-1 was highest in the preeclampsia group (p<0.001), whilst Ang-2 was highest in the normotensive pregnant group (p-=0.018). Plasma Tie-2 was highest in the PIH group. VEGF levels were significantly different between the preeclampsia group and the PIH group (p<0.05). Platelet VEGF levels were higher in the non-pregnant group than in the pregnant group, but there were no significant differences in the platelet levels of Ang-1 between the different groups. Ang-2, sFlt-1 and Tie-2 were undetectable in the platelet lysate in any of the patient groups or controls. Blood pressure was a major determinant of the different angiogenic factors studied. Abnormal indices of angiogenesis are evident in PIH and preeclampsia, with higher levels of sFlt-1 and lower levels ofVEGF; in PIH, increased levels of Ang-1 and Tie-2, but reduced Ang-2, are evident compared to normal pregnancy. These abnormalities may have implications for the pathogenesis of PIH and preeclampsia.

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Bhavina, K., J. Radhika et S. Sundara Pandian. « VEGF and eNOS Expression in Umbilical Cord from Pregnancy Complicated by Hypertensive Disorder with Different Severity ». BioMed Research International 2014 (2014) : 1–6. http://dx.doi.org/10.1155/2014/982159.

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Background. Reduced blood flow in hypertensive pregnancy may influence the production vasoconstrictors; subsequently the vessel remains in highly contracted state. NO is a vasodilator; VEGF influences its synthesis by regulating eNOS production. Aim of our study was to evaluate the expression of VEGF and eNOS in different severity of hypertensive pregnancy.Methods. Study was conducted in 4 groups with 40 members: group 1—control, group 2—gestational hypertension, group 3—mild preeclampsia, and group 4—severe preeclampsia. Fetal end of umbilical cord was taken and follows IHC staining protocol for VEGF and eNOS antibody. Staining intensity were measured by semiquantitative scoring method. Mann WhitneyUtest was used to compare each group.Results. Decreased expression of both VEGF and eNOS was found in hypertensive condition than in normal condition. Among hypertensive group, severe preeclamptic group showed more intensity in staining than gestational hypertension and mild preeclampsia.Conclusion. Reduction of VEGF and eNOS in gestational hypertension may lead to hypoperfusion and subsequent hypoxia of fetus in hypertensive pregnancy. The developed hypoxic state may upregulate the synthesis of VEGF and thereby eNOS. Increased expression of VEGF and eNOS in severe group may be a compensatory mechanism to dilate the blood vessels and to improve blood flow of fetus.

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Corrêa, Isis Paloppi, Rodrigo Ruano, Nilton Hideto Takiuti, Rossana Pulcinelli Vieira Francisco, Estela Bevilacqua et Marcelo Zugaib. « Expression of angiogenic factors in placenta of stressed rats ». Reproduction, Fertility and Development 24, n^o 6 (2012) : 851. http://dx.doi.org/10.1071/rd11202.

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The aim of the present study was to analyse the influence of stress on pregnant rats, particularly in terms of maternal, placental and fetal weight, placental morphology and placental gene expression of the angiogenic factors Vegfa and Pgf and their receptors. The parameters were evaluated on gestation Day 20. Maternal, fetal and placental weights were statistically lower in stressed animals than controls, suggesting abnormalities in gestational physiology. Morphologically the placentas of rats subjected to stress were reduced in size and weight, with few glycogen cells and a significant increase in the number of apoptotic cells. Stress caused an increase in placental gene expression of Vegfa (P < 0.05) and a reduction in Pgf, Flt1 and Kdr expression (P < 0.05). It has been suggested that increased VEGF is associated with vasodilatation and hypotension, but in this model persistent hypertension was present. This study suggests that the limited hypotensive Vegfa response to stress-induced hypertension could result from reduced expression of Flt1/Kdr disrupting specific VEGF pathways. These findings may elucidate one of the multiple possible factors underlying how stress modulates placental physiology, and could aid the understanding of stress-induced gestational disorders.

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Feng, Yan, Ying Li, Xinling Yang, Limin Han, Luning Wang, Shan Gao, Ruixue Yin et al. « Direct evidence of VEGF-mediated neuroregulation and afferent explanation of blood pressure dysregulation during angiogenic therapy ». Frigid Zone Medicine 1, n^o 2 (1 décembre 2021) : 119–26. http://dx.doi.org/10.2478/fzm-2021-0015.

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Abstract Objective Oncocardiology is increasingly hot research field/topic in the clinical management of cancer with anti-angiogenic therapy of vascular endothelial growth factor (VEGF) that may cause cardiovascular toxicity, such as hypertension via vascular dysfunction and attenuation of eNOS/NO signaling in the baroreflex afferent pathway. The aim of the current study was to evaluate the potential roles of VEGF/VEGF receptors (VEGFRs) expressed in the baroreflex afferent pathway in autonomic control of blood pressure (BP) regulation. Methods The distribution and expression of VEGF/VEGFRs were detected in the nodose ganglia (NG) and nucleus of tractus solitary (NTS) using immunostaining and molecular approaches. The direct role of VEGF was tested by NG microinjection under physiological and hypertensive conditions. Results Immunostaining data showed that either VEGF or VEGFR2/VEGFR3 was clearly detected in the NG and NTS of adult male rats. Microinjection of VEGF directly into the NG reduced the mean blood pressure (MBP) dose-dependently, which was less dramatic in renovascular hypertension (RVH) rats, suggesting the VEGF-mediated depressor response by direct activation of the 1st-order baroreceptor neurons in the NG under both normal and disease conditions. Notably, this reduced depressor response in RVH rats was directly caused by the downregulation of VEGFR2, which compensated the up regulation of VEGF/VEGFR3 in the NG during the development of hypertension. Conclusion It demonstrated for the first time that the BP-lowering property of VEGF/VEGFRs signaling via the activation of baroreflex afferent function may be a common target/pathway leading to BP dysregulation in anti-angiogenic therapy.

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Abraldes, Juan G., Yasuko Iwakiri, Mauricio Loureiro-Silva, Omar Haq, William C. Sessa et Roberto J. Groszmann. « Mild increases in portal pressure upregulate vascular endothelial growth factor and endothelial nitric oxide synthase in the intestinal microcirculatory bed, leading to a hyperdynamic state ». American Journal of Physiology-Gastrointestinal and Liver Physiology 290, n^o 5 (mai 2006) : G980—G987. http://dx.doi.org/10.1152/ajpgi.00336.2005.

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Increased nitric oxide (NO) is the main factor leading to the hyperdynamic circulation associated with advanced portal hypertension (PHT), but the initial mechanisms and the magnitude of increase in portal pressure required to trigger NO production are not known. We addressed these issues by studying systemic and splanchnic hemodynamics and endothelial NO synthase (eNOS) and VEGF expression in rats with different degrees of portal hypertension. Portal vein ligation (PVL) performed over needles of three different calibers (16-, 18-, and 20-gauge) yielded different degrees of PHT and portosystemic shunting. Compared with sham rats, all three groups of PVL rats exhibited features of hyperdynamic circulation. Rats with minimal portal hypertension (PVL with a 16-gauge needle) showed an early increase in VEGF and eNOS expression selectively at the jejunum. Immunofluorescence showed that VEGF expression was located in highly vascularized areas of the mucosa. Inhibition of VEGF signaling markedly attenuated the increase in eNOS expression. In conclusion, mild increases in portal pressure are enough to upregulate eNOS at the intestinal microcirculation, and this occurs, at least in part, through VEGF upregulation.

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Escalante, Carmen P., et Ali Zalpour. « Vascular Endothelial Growth Factor Inhibitor-Induced Hypertension : Basics for Primary Care Providers ». Cardiology Research and Practice 2011 (2011) : 1–8. http://dx.doi.org/10.4061/2011/816897.

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Frequently, primary care providers continue to manage the overall medical care of cancer patients. With newer and often more potent antitumor agents, patients may present to their local physicians with drug-induced toxicities such as hypertension induced by vascular endothelial growth factor (VEGF) inhibitors. It is imperative that these healthcare providers are aware of basic aspects of this drug class, as its use has increased significantly in the last several years. Uncontrolled or malignant hypertension due to these agents should be recognized readily and treated early to prevent more severe outcomes. This overview provides a brief background on the role of VEGF and angiogenesis in tumor metabolism as well as theories of the mechanism of VEGF inhibitors and hypertension. Helpful clinical practice aspects including the types of inhibitors used in the United States and their pharmacologic characteristics will be discussed. Also, diagnosis and treatment of hypertension induced by vascular endothelial growth factors are reviewed. A summary of key aspects of this drug class and hypertension is included.

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Nemtsova, Valeriya D., Olena V. Vysotska, Hanna M. Strashnenko, Hanna M. Borodkina, Tetiana O. Utytskykh et Yurii P. Balym. « PROGNOSTIC ROLE OF VASCULAR ENDOTHELIAL GROWTH FACTOR IN THE CARDIOVASCULAR COMPLICATIONS DEVELOPMENT IN PATIENTS WITH POLYMORBID PATHOLOGY : THE COMBINED COURSE OF HYPERTENSION, TYPE 2 DIABETES MELLITUS AND SUBCLINICAL HYPOTHYROIDISM ». Wiadomości Lekarskie 75, n^o 12 (2022) : 3025–30. http://dx.doi.org/10.36740/wlek202212122.

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The aim: To determine the prognostic value of vascular endothelial growth factor (VEGF) levels for the development of cardiovascular complications in patients with a combined course of hypertension, type 2 diabetes mellitus and subclinical hypothyroidism. Materials and methods: 93 patients (mean age 61,71±0,87 years) with the combined course of hypertension, type 2 diabetes mellitus and subclinical hypothyroidism were examined. Parameters of lipid, carbohydrate metabolism, plasma insulin, VEGF (by ELISA), blood pressure levels were measured. Observation period was12 months. Results: VEGF levels in the patients group were significantly higher than in the controls (482,77±21,34 pg/ ml vs. 121,84±11,66 pg/ ml, p <0,001). The results of the ROC analysis made it possible to propose the level of VEGF ≥ 512.31 pg/ml as an identifier for the cardiovascular complications development in patients with studied comorbidity. VEGF levels in patients who developed cardiovascular complications during observation period were significantly higher the VEGF threshold levels (650,76 ± 52,04 pg / ml vs. 512,31 pg/ml, respectively, p = 0,038) and VEGF levels in patients without cardiovascular complications were significantly lower the threshold values (420,47± 21,67 pg/ml vs. 512,31 pg/ml, respectively, p = 0,047). Conclusions: Determination of the vascular endothelial growth factor plasma level allows to evaluate the long-term prognosis in comorbid course of hypertension, type 2 diabetes mellitus and subclinical hypothyroidism.

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Zhang, Huiying, et Lei Zheng. « PM2.5 is a risk factor of hypertension : A study on regression model for risk factors of hypertension ». Materials Express 12, n^o 9 (1 septembre 2022) : 1241–46. http://dx.doi.org/10.1166/mex.2022.2225.

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Objective: In this prospective observational research, we aimed to explore the association among PM2.5 concentration, hypertension and clinical factors in Taiyuan at different times by regression analysis. Methods: This prospective observational research enrolled 95 cases with hypertension and 98 healthy individuals who went to our hospital during March 2017 to September 2018. PM2.5 concentrations data were collected from the national urban air quality report released by China environmental monitoring station. Age, BMI and sex of all subjects were recorded. DBP, SBP, cytokines and VEGF, ANG-2, white blood cells (WBC), fibrinogen (Fib), fasting plasma glucose (FPG) and lipid metabolic factors levels of all subjects were collected in the first week of each month during November 2018 to October 2019. Results: The PM2.5 concentration of winter spring (WS) group were remarkably increased than that in summary autumn (SA) group. Meanwhile, the SBP and DBP of patients with hypertension in WS group were markedly elevated than that in SA group. Similar results were showed in the healthy volunteers. The TNF-α, IL-6, IL-1β, VEGF, Fib and TC levels of patients with hypertension in WS group were dramatically enhanced than the SA group. Positive correlation was observed between PM2.5 concentration and IL-6, VEGF, FPG, IL-1β and TC. PM2.5 concentration and FPG, TC, TG, IL-6, VEGF were the risk factors for hypertension. Conclusion: This study showed that SBP and DBP increased when PM2.5 concentration raised. PM2.5 concentration was related to the clinical factors of patients with hypertension.

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Gu, Jian-Wei, R. Davis Manning, Emily Young, Megan Shparago, Brandi Sartin et Amelia Purser Bailey. « Vascular endothelial growth factor receptor inhibitor enhances dietary salt-induced hypertension in Sprague-Dawley rats ». American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 297, n^o 1 (juillet 2009) : R142—R148. http://dx.doi.org/10.1152/ajpregu.90972.2008.

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Clinical evidence links the inhibition of VEGF to hypertension. However, the mechanisms by which VEGF affects the pathogenesis of hypertension remain in question. We determined 1) whether administration of VEGF receptor inhibitor SU5416 enhances dietary salt-induced hypertension in Sprague-Dawley (SD) rats, and 2) whether VEGF or SU5416 directly affects proliferation of cultured human renal proximal tubular epithelial cells (HRPTEC) and endothelial nitric oxide synthase (eNOS) expression in cultured human glomerular microvessel endothelial cells (HGMEC). Ten 10-wk-old male SD rats received a high sodium diet (HS; 8%) and the other 10 SD rats received a normal sodium diet (NS; 0.5%) for 4 wks. After 2 wks of the dietary program, five rats were administered with SU5416 at 10 mg·kg−1·day−1 ip or DMSO (vehicle) for 14 days in HS and NS groups. Mean arterial pressure was significantly higher in rats treated with SU5416, as opposed to those treated with DMSO and fed with HS for 4 wk (157.6 ± 3.9 vs. 125.9 ± 4.3 mmHg, P < 0.01). Increased proteinuria and albuminuria were associated with marked renal histological abnormalities in HS group with SU5416 administration, compared with those in the vehicle HS group. 3H-thymidine incorporation assay showed that SU5416 blocked the actions of both exogenous and endogenous VEGF on the proliferation of HRPTEC. VEGF (10 ng/ml) significantly increased eNOS protein levels by 29% in cultured HGMEC, but its action was completely abolished by SU5416. These results suggest that VEGF receptor inhibition enhances dietary salt-induced hypertension and kidney injury, possibly by direct damage on renal cells and decreasing NO production by eNOS.

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Kneedler, Sterling C., Lauren E. Phillips, Kayla R. Hudson, Katharine M. Beckman, Catalina A. Lopez Gelston, Joseph M. Rutkowski, Alan R. Parrish, Peter A. Doris et Brett M. Mitchell. « Renal inflammation and injury are associated with lymphangiogenesis in hypertension ». American Journal of Physiology-Renal Physiology 312, n^o 5 (1 mai 2017) : F861—F869. http://dx.doi.org/10.1152/ajprenal.00679.2016.

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Lymphatic vessels are vital for the trafficking of immune cells from the interstitium to draining lymph nodes during inflammation. Hypertension is associated with renal infiltration of activated immune cells and inflammation; however, it is unknown how renal lymphatic vessels change in hypertension. We hypothesized that renal macrophage infiltration and inflammation would cause increased lymphatic vessel density in hypertensive rats. Spontaneously hypertensive rats (SHR) that exhibit hypertension and renal injury (SHR-A3 strain) had significantly increased renal lymphatic vessel density and macrophages at 40 wk of age compared with Wistar-Kyoto (WKY) controls. SHR rats that exhibit hypertension but minimal renal injury (SHR-B2 strain) had significantly less renal lymphatic vessel density compared with WKY rats. The signals for lymphangiogenesis, VEGF-C and its receptor VEGF-R3, and proinflammatory cytokine genes increased significantly in the kidneys of SHR-A3 rats but not in SHR-B2 rats. Fischer 344 rats exhibit normal blood pressure but develop renal injury as they age. Kidneys from 24-mo- and/or 20-mo-old Fischer rats had significantly increased lymphatic vessel density, macrophage infiltration, VEGF-C and VEGF-R3 expression, and proinflammatory cytokine gene expression compared with 4-mo-old controls. These data together demonstrate that renal immune cell infiltration and inflammation cause lymphangiogenesis in hypertension- and aging-associated renal injury.

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Purwani, Rani, Eti Yerizel et Efrida . « The Effect of the Extra Virgin Olive Oil Administration towards the Malondialdehyde and Vascular Endothelial Growth Factor Levels on the Hypertensive Pregnant Rats ». International Journal of Research and Review 9, n^o 6 (23 juin 2022) : 238–44. http://dx.doi.org/10.52403/ijrr.20220626.

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Background: Hypertension and pregnancy cause placental ischemia which will produce the toxic free radicals that cause the oxidative stress and increase the malondialdehyde (MDA) level. Oxidative stress also decreases the Vascular Endothelial Growth Factor (VEGF) level. Extra Virgin Olive Oil (EVOO) contains antioxidants that can break free radical chain reactions. This study aims to determine the effect of the EVOO administration on the MDA and VEGF levels on the hypertensive pregnant rats. Methods: A post-test only control group design study was conducted on 30 pregnant rats consisting of a negative control group (K-), a positive control group (K+) and 3 treatment groups as a hypertension model (Pl, P2, P3), NaC1-induced hypertension model 6 % on day 6 to day 12 of pregnancy. All treatment groups were given EVOO except K+, from day 13 to day 19. On day 20, all the rats were executed. The MDA examination used a spectrophotometer and the VEGF examination used ELISA. The data was tested by using the one way ANOVA test which was statistically significant if p < 0.05. Results: The results of this study showed that there was a significant decrease on the mean of the MDA level after the EVOO administration, especially in the P3 group, which was 1,532 mmol/l (p 0.000) and a significant increase on the mean of the VEGF level after the EVOO administration, especially in the P3 group, which was 68,892 ng/l. (p 0.000). It means that there is an effect of the EVOO administration on the MDA and VEGF levels of hypertensive pregnant rats. Conclusion: The conclusion of this study is that the EVOO administration can decrease the MDA level and increase the VEGF level on hypertensive pregnant rats. Keywords: EVOO, MDA, VEGF, Hypertension.

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Kang, Duk-Hee, Yoon-Goo Kim, Takeshi F. Andoh, Katherine L. Gordon, Shin-Ichi Suga, Marilda Mazzali, J. Ashley Jefferson et al. « Post-cyclosporine-mediated hypertension and nephropathy : amelioration by vascular endothelial growth factor ». American Journal of Physiology-Renal Physiology 280, n^o 4 (1 avril 2001) : F727—F736. http://dx.doi.org/10.1152/ajprenal.2001.280.4.f727.

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Recent studies have demonstrated a role for microvascular and tubulointerstitial injury in some models of salt-sensitive hypertension. We utilized a model of post-cyclosporin A (CsA) nephropathy and hypertension to test the hypothesis that treatment with an angiogenic factor aimed at ameliorating the microvascular and renal injury would prevent the development of hypertension. CsA was administered with a low-salt diet for 45 days, resulting in a renal lesion characterized by afferent arteriolopathy, focal peritubular capillary loss, and tubulointerstitial fibrosis. Rats were then placed on a high-salt diet and randomized to receive either vascular endothelial growth factor (VEGF121) or vehicle for 14 days. Placement of rats with established CsA nephropathy on a high-salt diet results in the rapid development of salt-sensitive hypertension. VEGF121 treatment resulted in lower blood pressure, and this persisted on discontinuing the VEGF. VEGF121 treatment was also associated with a decrease in osteopontin expression, macrophage infiltration, and collagen III deposition and markedly stimulated resolution of the arteriolopathy (20.9 ± 7.8 vs. 36.9 ± 6.1%, VEGF vs. vehicle, P < 0.05). In conclusion, CsA-associated renal microvascular and tubulointerstitial injury results in the development of salt-sensitive hypertension. Treatment of animals with established CsA nephropathy with VEGF reduces the hypertensive response and accelerates histological recovery. The vascular protective effect of VEGF may be due to the improvement of arteriolopathy. Angiogenic growth factors may represent a novel strategy for treating CsA-associated hypertension and renal disease.

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Neves, Karla B., Augusto C. Montezano, Ninian N. Lang et Rhian M. Touyz. « Vascular toxicity associated with anti-angiogenic drugs ». Clinical Science 134, n^o 18 (septembre 2020) : 2503–20. http://dx.doi.org/10.1042/cs20200308.

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Abstract Over the past two decades, the treatment of cancer has been revolutionised by the highly successful introduction of novel molecular targeted therapies and immunotherapies, including small-molecule kinase inhibitors and monoclonal antibodies that target angiogenesis by inhibiting vascular endothelial growth factor (VEGF) signaling pathways. Despite their anti-angiogenic and anti-cancer benefits, the use of VEGF inhibitors (VEGFi) and other tyrosine kinase inhibitors (TKIs) has been hampered by potent vascular toxicities especially hypertension and thromboembolism. Molecular processes underlying VEGFi-induced vascular toxicities still remain unclear but inhibition of endothelial NO synthase (eNOS), reduced nitric oxide (NO) production, oxidative stress, activation of the endothelin system, and rarefaction have been implicated. However, the pathophysiological mechanisms still remain elusive and there is an urgent need to better understand exactly how anti-angiogenic drugs cause hypertension and other cardiovascular diseases (CVDs). This is especially important because VEGFi are increasingly being used in combination with other anti-cancer dugs, such as immunotherapies (immune checkpoint inhibitors (ICIs)), other TKIs, drugs that inhibit epigenetic processes (histone deacetylase (HDAC) inhibitor) and poly (adenosine diphosphate-ribose) polymerase (PARP) inhibitors, which may themselves induce cardiovascular injury. Here, we discuss vascular toxicities associated with TKIs, especially VEGFi, and provide an up-to-date overview on molecular mechanisms underlying VEGFi-induced vascular toxicity and cardiovascular sequelae. We also review the vascular effects of VEGFi when used in combination with other modern anti-cancer drugs.

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Sandrim, V. C., M. R. Luizon, T. C. Izidoro-Toledo, E. B. Coelho, H. Moreno et J. E. Tanus-Santos. « Functional VEGF haplotypes affect the susceptibility to hypertension ». Journal of Human Hypertension 27, n^o 1 (22 décembre 2011) : 31–37. http://dx.doi.org/10.1038/jhh.2011.110.

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Situmorang, Putri Cahaya, Syafruddin Ilyas, Doni Aldo Samuel Siahaan, Martina Restuati, Endang Ratna Sari, Chairunisa Chairunisa et Muhammad Faldhy Maliki. « Effect of Rhodomyrtus tomentosa Hassk. on HIF1α and VEGF expressions on hypertension placental ». Journal of Pharmacy & ; Pharmacognosy Research 10, n^o 6 (1 novembre 2022) : 1076–86. http://dx.doi.org/10.56499/jppres22.1517_10.6.1076.

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Context: HIF1α and VEGF are proteins marker oxidative stress and a decrease in placental growth factor (PlGF). Decreasing of HIF1α and VEGF in rats displayed poor trophoblast differentiation, placental abnormalities, and fetal mortality. Rhodomyrtus tomentosa is a flowering plant in the Myrtaceae family that has the potential to be a source of health-promoting chemicals. Aims: To analyze HIF1α and VEGF in serum and hypertension placental tissue after giving Rhodomyrtus tomentosa (RHO) leaves extract. Methods: Six treatments were given to the rats that were identified as being pregnant and pregnant rats with hypertension were given RHO with three doses: (a) normal pregnant rats (control); (b) hypertensive rats; (c) hypertensive rats + 100 mg/kg BW of RHO; (d) hypertensive rats +200 mg/kg BW of RHO; and (e) hypertensive rats + 400 mg/kg BW of RHO and (f) hypertensive rats + nifedipine. Under ketamine anesthesia, pregnant rats were removed on their 20th day of gestation. Immunohistochemistry and ELISA were used to assess HIF1α and VEGF protein expression. Results: There was a significant difference (p<0.01) in the expression of HIF1α and VEGF in the labyrinthine zone and yolk sac of the rat placenta between the normal (C-) and hypertensive (C+) groups. HIF1α and VEGF expression decreased when RHO was administered at doses ranging from 100 to 400 mg/kg BW. However, there was no significant change (p>0.05) in VEGF expression in the basal zone of the rat placenta across all groups. Conclusions: Rhodomyrtus tomentosa leaves extract decreases HIF1α and VEGF expressions in serum and repairs the tissue of the placenta's labyrinth, basal, and yolk sacs.

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Mahmoud, Estabraq A. « Expression of Vascular Endothelial Growth Factor in the Placenta of Iraqi Women Complicated with Hypertensive Disorder ». INTERNATIONAL JOURNAL OF DRUG DELIVERY TECHNOLOGY 12, n^o 03 (30 juin 2022) : 977–80. http://dx.doi.org/10.25258/ijddt.12.3.09.

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During pregnancy, high blood pressure disorder is the most common medical complication in pregnancy. It is the foremost cause of maternal mortality and perinatal diseases. Vascular endothelial growth factor (VEGF) affects the growth of vascular endothelial cells, existence, and multiplying, which are known to be expressed in the human placenta. This study aimed to identify the expression VEGF in the placenta of hypertension and normotensive women. In this study, a cross-sectional study from november 2019 to February 2020. A total of 100 placentae involved 50 hypertensive cases and 50 normotensive groups were assessed. VEGF-A expression in two placentas groups was evaluated by immunohistochemistry techniques. Strong and moderate VEGF expression was seen in syncytiotrophoblasts, stromal and endothelial cells of hypertensive cases, while not seen in hypertensive cases. There were statistically significant differences in VEGF-A expression between hypertensive cases and normotensive group. In conclusion, VEGF-A expression was significantly increased in each of syncytiotrophoblasts, stroma and endothelial cells in the placenta of hypertensive cases, and it could be used to predict the development of hypertension.

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Dhami, Abhinav, Latha Vichu et Parveen Sen. « Macular edema secondary to malignant Hypertension managed with Intravitreal Bevacizumab ». Nepalese Journal of Ophthalmology 11, n^o 1 (3 septembre 2019) : 98–101. http://dx.doi.org/10.3126/nepjoph.v11i1.25444.

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Introduction: Intravitreal anti VEGF agents are used in a variety of retinal pathologies to decrease the VEGF levels resulting due to breakdown of the blood retinal barrier hence decrease the exudation from vessels which causes macular edema (ME). Case: A 61year old patient presented with sudden decrease in vision in both eyes with a history of systemic malignant hypertension leading to macular edema as documented on optical Coherence Tomography (OCT) in both eyes. The foveal thickness (FT)of 536 and 328 microns (μ) were observed in the right and left eye each. He was advised intravitreal anti vascular endothelial growth factor (VEGF) in both eyes and advised complete systemic evaluation with the physician. Following one month postintravitreal bevacizumab ( IVB) injection in right eye, marked visual improvement was noted with concomitant significant reduction in macular edema in both eyes. Observation: Single Bevacizumab injection with control of hypertension in our patient resulted in rapid resolution of the macular edema and early visual recovery. Intravitreal anti VEGF is an effective treatment option in eyes due to hypertensivemaculopathy especially to gain speedy visual recovery. Conclusion: The case gives a unique outlook to the course of ME in the single patient with malignant HTN with or without IVB injection. We believe that anti VEGF injections may result in rapid recovery in vision and minimize the risk of permanent vision loss in eyes with malignant hypertension.

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Chongsrisawat, Voranush, Paisarn Vejchapipat et Yong Poovorawan. « Serum vascular endothelial growth factor per platelet count in patients with biliary atresia ». Asian Biomedicine 4, n^o 2 (1 avril 2010) : 223–29. http://dx.doi.org/10.2478/abm-2010-0030.

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Abstract Background: Biliary atresia (BA) is a progressive, sclerosing, inflammatory process resulting in complete obliteration of the extrahepatic bile ducts. The obstruction of bile flow engenders worsening cholestasis, hepatic fibrosis, and cirrhosis, which lead to portal hypertension and a decline in hepatic synthetic function. Hepatic stellate cells, which play roles in hepatic fibrogenesis, are an important source of various inflammatory mediators including vascular endothelial growth factor (VEGF) in the injured liver. Objectives: Investigate the level of serum VEGF and serum VEGF per platelet count in patients with BA and its relation to clinical characteristics. Methods: Peripheral blood samples were taken from 70 BA patients and 15 healthy control children. Serum VEGF was measured by enzyme-linked immunosorbent assay. We compared serum VEGF and serum VEGF per platelet count in BA patients with the respective results obtained in healthy control children. The relation of serum VEGF per platelet count with clinical variables of BA patients was investigated. Results: Serum VEGF levels and serum VEGF per platelet count in BA patients were not significantly different from those in normal controls (289.64±230.01 pg/mL vs. 312.36±189.05 pg/mL; p=0.72 and 1.72±1.21x106 vs. 1.57±0.97x106; p=0.66). Significant differences were observed among BA patients when VEGF per platelet count was categorized by the presence of esophageal varice (p=0.03). Only in BA patients was the serum level of VEGF correlated with the number of platelets (r=0.53, p<0.001). Conclusion: A high serum VEGF per platelet count is a useful marker for the development of portal hypertension in BA patients, especially for esophageal varice. Serum VEGF per platelet count may be useful for monitoring disease course in BA after hepatic portoenterostomy.

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Tew, W. P., N. Colombo, I. Ray-Coquard, A. Oza, J. del Campo, G. Scambia et D. Spriggs. « VEGF-Trap for patients (pts) with recurrent platinum-resistant epithelial ovarian cancer (EOC) : Preliminary results of a randomized, multicenter phase II study ». Journal of Clinical Oncology 25, n^o 18_suppl (20 juin 2007) : 5508. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.5508.

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5508 Background: Vascular endothelial growth factor (VEGF) is over-expressed in EOC and associated with poor prognosis. VEGF Trap, a potent angiogenesis inhibitor fusion protein, is comprised of portions of human VEGF-receptor R1+R2 (Flt-1, KDR) extracellular domains and fused to the Fc portion of human IgG. VEGF Trap binds VEGF-A and neutralizes all VEGF-A isoforms plus placental growth factor. Methods: This is a randomized, double blind, multicenter, 2-stage, phase II trial of VEGF Trap (2 or 4 mg/kg) administered intravenously every 2 weeks, in pts with recurrent EOC. Eligible criteria included 2 or 3 prior chemo regimens for advanced disease; platinum- resistance, topotecan- and/or liposomal doxorubicin-resistance; no prior VEGF inhibitor treatment; ECOG performance status 0–2; normal organ function; no proteinuria (<500 mg/24hrs or UPCR =1); controlled blood pressure. This Simon 2 stage design, requires 3 responders out of 42 evaluable, in each arm to continue accrual into stage 2. Results: Across 62 centers in Europe, Canada and US, rapid accrual led to 162 pts randomized from 5/06 to 12/06. Median age: 58, PS (0,1,2): 56,40,4%. Of 45 pts currently in the database, across the two arms, adverse events included (any grade): headache (38%), fatigue (36%), dysphonia (33%), nausea (29%), asthenia (24%), diarrhea (18%), hypertension (16%), proteinuria (7%), renal dysfunction (4%). Grade 3–4, included: hypertension (9%), proteinuria (4%), encephalopathy (2%) and renal failure (2%). Of the 162 pts who had at minimum one cycle, study drug-related SAE include (N): thrombocytopenia (1), anemia (1), headache (1) asthenia (2),dyspnea (1), hypertension (4), bowel perforation (2), encephalopathy (1), renal failure (2), proteinuria (1), phlebitis (1) and pulmonary embolism (1). 5 partial responses (11%) have been reported. Conclusions: VEGF Trap has activity in this heavily-pretreated EOC population. The first stage of accrual is complete and updated results will be presented. No significant financial relationships to disclose.

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Langenberg, Marlies H. G., Carla M. L. van Herpen, Johann De Bono, Jan H. M. Schellens, Clemens Unger, Klaas Hoekman, Hubert E. Blum et al. « Effective Strategies for Management of Hypertension After Vascular Endothelial Growth Factor Signaling Inhibition Therapy : Results From a Phase II Randomized, Factorial, Double-Blind Study of Cediranib in Patients With Advanced Solid Tumors ». Journal of Clinical Oncology 27, n^o 36 (20 décembre 2009) : 6152–59. http://dx.doi.org/10.1200/jco.2009.22.2273.

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Purpose Hypertension is a commonly reported adverse effect after administration of vascular endothelial growth factor (VEGF) inhibitors. Cediranib is a highly potent and selective VEGF signaling inhibitor of all three VEGFRs. This study prospectively investigated hypertension management to help minimize dose interruptions/reductions to maximize cediranib dose intensity. Patients and Methods Patients (n = 126) with advanced solid tumors were randomly assigned to one of four groups: cediranib 30 or 45 mg/d with or without antihypertensive prophylaxis. All patients developing hypertension on cediranib treatment were treated with a standardized, predefined hypertension management protocol. Results Cediranib was generally well tolerated, and all groups achieved high-dose intensities in the first 12 weeks (> 74% in all groups). Antihypertensive prophylaxis did not result in fewer dose reductions or interruptions. Increases in blood pressure, including moderate and severe readings of hypertension, were seen early in treatment in all groups and successfully managed. Severe hypertension occurred in one patient receiving prophylaxis versus 18 in the nonprophylaxis groups. Overall, there were nine partial responses, and 38 patients experienced stable disease ≥ 8 weeks. Conclusion To our knowledge, this is the first prospective investigation of hypertension management during administration of a VEGF signaling inhibitor. All four regimens were well tolerated with high-dose intensities and no strategy was clearly superior. The current cediranib hypertension management protocol appears to be effective in managing hypertension compared with previous cediranib studies where no plan was in place, and early recognition and treatment of hypertension is likely to reduce the number of severe hypertension events. This protocol is included in all ongoing cediranib clinical studies.

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Steeghs, N., T. J. Rabelink, J. op ’t Roodt, E. de Koning et H. Gelderblom. « Bevacizumab-related hypertension : Search for underlying mechanisms ». Journal of Clinical Oncology 27, n^o 15_suppl (20 mai 2009) : e14520-e14520. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.e14520.

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e14520 Background: Hypertension is a commonly observed side effect of inhibitors of VEGF/VEGFR-2 signaling such as bevacizumab. The mechanisms leading to this increase in blood pressure during anti-angiogenic therapy have not been elucidated. Recent studies suggest that functional rarefaction (a decrease in perfused microvessels) or anatomic rarefaction (a reduction in capillary density) may play an important role. The purpose of this study was to search for possible mechanisms that cause hypertension in patients treated with anti-angiogenic therapy and to confirm our hypothesis that systemic inhibition of VEGF inhibits vascular function and causes rarefaction. Methods: Patients treated with bevacizumab for any type of cancer were eligible. Measurements of blood pressure, flow-mediated dilatation (FMD), nitroglycerin-mediated dilatation (NMD), aortic pulse wave velocity (PWV), and capillary density and diameter with sidestream dark field (SDF) imaging of the mucosal microcirculation of the lip were performed at baseline, after 6 weeks of treatment, and 3 months after discontinuation of bevacizumab treatment. Results: Fourteen patients were included in this study. During bevacizumab treatment the mean systolic and diastolic blood pressure values increased, +3.4 mmHg (p=0.406), and +5.6 mmHg (p=0.023) resp. Mean FMD showed a statistically significant decrease of -3.1% (p=0.006). Mean NMD was unchanged. After 6 weeks treatment mean PWV increased significantly +0.7 m/s (p=0.0.027). A significant reduction in capillary density was seen from 18.0 capillary loops per image at baseline to 12.7 after 6 weeks (p=0.000007). Also a significant reduction in capillary diameter was seen, from 6.9 to 5.6 μm (p=0.002). Results after discontinuation of bevacizumab treatment were not yet available. Conclusions: Rarefaction (reduction in capillary density) and endothelial dysfunction observed in this study provide a plausible mechanism for the increase in blood pressure which results from treatment with bevacizumab. No significant financial relationships to disclose.

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Diao, Xiaoyan, Kun Ding et Xuemei Ma. « Efficacy of normodyne-magnesium sulfate combination treatment on pregnancy-induced hypertension, and its effect on VEGF and Flt-1 levels ». Tropical Journal of Pharmaceutical Research 20, n^o 10 (21 novembre 2021) : 2155–61. http://dx.doi.org/10.4314/tjpr.v20i10.20.

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Purpose: To investigate the efficacy of the combined use of normodyne and magnesium sulfate in the treatment of pregnancy-induced hypertension, and its effect on vascular endothelial growth factor (VEGF) and factor receptor-1 (Flt-1) levels in serum.Methods: A total of 100 patients with pregnancy-induced hypertension attending Maternal and Child Health Hospital of Xinjiang Uygur Autonomous Region, Xinjiang, China, were categorized as Group A, and then further subdivided into control sub-group (who were treated with magnesium sulfate only) and study sub-group (treated with magnesium sulfate plus normodyne). Furthermore, 100 healthy pregnantwomen attending the hospital for prenatal examination during the same period were categorized as Group B. Serum expressions of VEGF and Flt-1 in all patients were determined and compared. The therapeutic effect, adverse reactions, adverse pregnancy outcomes, blood pressure before and after treatment, 24 h proteinuria, and serum expression levels of VEGF and Flt-1 in the study and control groups were determined and compared.Results: Serum VEGF levels in patients with pregnancy-mediated hypertension were significantly lower than those of healthy pregnant women, and Flt-1 was raised in healthy pregnant women (p < 0.05). In the study group, treatment was markedly more effective, and the degree of amelioration of blood pressure, 24 h proteinuria, serum VEGF, and Flt-1 were significantly higher than for control sub-group. There were lower adverse pregnancy outcomes in study sub-group than in control (p < 0.05).Conclusion: The combination of magnesium sulfate and normodyne produces greater clinical efficacy in the treatment of patients with pregnancy-induced hypertension than magnesium sulfate alone, and also shows a high safety profile.

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Partovian, Chohreh, Serge Adnot, Saadia Eddahibi, Emmanuel Teiger, Micheline Levame, Patrick Dreyfus, Bernadette Raffestin et Christian Frelin. « Heart and lung VEGF mRNA expression in rats with monocrotaline- or hypoxia-induced pulmonary hypertension ». American Journal of Physiology-Heart and Circulatory Physiology 275, n^o 6 (1 décembre 1998) : H1948—H1956. http://dx.doi.org/10.1152/ajpheart.1998.275.6.h1948.

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Vascular endothelial growth factor (VEGF) is an endothelial cell-specific mitogen that is upregulated during exposure to hypoxia. In this study, we analyzed heart and lung VEGF mRNA expression and examined pulmonary vascular remodeling as well as myocardial capillary density in two rat models of pulmonary hypertension involving exposure to chronic hypoxia (CH) and treatment with monocrotaline (MCT), respectively. The rats were studied after 0.5, 1, 3, 15, and 30 days of exposure to 10% O2 or 1, 6, and 30 days after a subcutaneous MCT injection (60 mg/kg). Both CH and MCT induced pulmonary hypertension and hypertrophy of the right ventricle (RV) with increased RV weight and atrial natriuretic peptide mRNA expression. VEGF mRNA expression as assessed by Northern blot analysis was potently induced after 12 h of hypoxia in both the right and left ventricles. After prolonged exposure to hypoxia, VEGF mRNA returned to baseline in the left ventricle (LV) but remained increased in the RV, where it peaked after 30 days. In MCT rats, VEGF mRNA was unchanged in the LV but decreased by 50% in the RV and by 90% in the lungs after 30 days. VEGF mRNA remained unchanged in the lungs from CH rats. Pulmonary vascular remodeling was more pronounced in MCT than in CH rats. The number of capillaries per RV myocyte was increased in rats exposed to 30 days of hypoxia, whereas it remained unchanged in MCT rats despite a similar degree of RV hypertrophy. Our results suggest that the sustained increase in VEGF expression in the hypertrophied RV during CH may account for the increased number of capillaries per myocyte. In contrast, reduced VEGF expression in the lungs and RV of MCT rats may aggravate pulmonary vascular remodeling and compromise RV myocardial perfusion.

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Schneider, Bryan P., Molin Wang, Milan Radovich, George W. Sledge, Sunil Badve, Ann Thor, David A. Flockhart et al. « Association of Vascular Endothelial Growth Factor and Vascular Endothelial Growth Factor Receptor-2 Genetic Polymorphisms With Outcome in a Trial of Paclitaxel Compared With Paclitaxel Plus Bevacizumab in Advanced Breast Cancer : ECOG 2100 ». Journal of Clinical Oncology 26, n^o 28 (1 octobre 2008) : 4672–78. http://dx.doi.org/10.1200/jco.2008.16.1612.

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Purpose No biomarkers have been identified to predict outcome with the use of an antiangiogenesis agent for cancer. Vascular endothelial growth factor (VEGF) genetic variability has been associated with altered risk of breast cancer and variable promoter activity. Therefore, we evaluated the association of VEGF genotype with efficacy and toxicity in E2100, a phase III study comparing paclitaxel versus paclitaxel plus bevacizumab as initial chemotherapy for metastatic breast cancer. Patients and Methods DNA was extracted from tumor blocks of patients from E2100. Three hundred sixty-three samples were available to evaluate associations between genotype and outcome. Genotyping was performed for selected polymorphisms in VEGF and VEGF receptor 2. Testing for associations between each polymorphism and efficacy and toxicity was performed. Results The VEGF-2578 AA genotype was associated with a superior median overall survival (OS) in the combination arm when compared with the alternate genotypes combined (hazard ratio = 0.58; 95% CI, 0.36 to 0.93; P = .023). The VEGF-1154 A allele also demonstrated a superior median OS with an additive effect of each active allele in the combination arm but not the control arm (hazard ratio = 0.62; 95% CI, 0.46 to 0.83; P = .001). Two additional genotypes, VEGF-634 CC and VEGF-1498 TT, were associated with significantly less grade 3 or 4 hypertension in the combination arm when compared with the alternate genotypes combined (P = .005 and P = .022, respectively). Conclusion Our data support an association between VEGF genotype and median OS as well as grade 3 or 4 hypertension when using bevacizumab in metastatic breast cancer.

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Tandon, Vibha, Swati Hiwale, Dnyanesh Amle, Tripti Nagaria et Pradeep Kumar Patra. « Assessment of Serum Vascular Endothelial Growth Factor Levels in Pregnancy-Induced Hypertension Patients ». Journal of Pregnancy 2017 (2017) : 1–5. http://dx.doi.org/10.1155/2017/3179670.

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Objective. The objective of the study was to assess the serum vascular endothelial growth factor (VEGF) levels in peripheral blood of patients with pregnancy-induced hypertension (PIH) and find association between serum VEGF levels and PIH.Methods. Thirty-five PIH subjects, 35 normal pregnant females, and 20 normal healthy females were included in the study. Detailed history, clinical examination, and relevant biochemical parameters were assessed; serum VEGF levels were estimated using Double-antibody enzyme-linked immunosorbent assay.Results. The study groups were found to be age matched (p=0.38). VEGF level in the pregnancy-induced hypertensive group (median = 109.19 (3.38±619)) was significantly higher than the normal pregnant (median = 20.82 (1.7–619)) and control (median = 4.92 (1.13–13.07)) group and the difference between these three groups was significant (p<0.0001). The 3 groups are found to be significantly different in terms of RBS (p=0.01), urea (p<0.0001), creatinine (p=0.0005), AST (p=0.0032), ALT (p=0.0007), total protein (p=0.0004), albumin (p<0.0001), calcium (p=0.001), and sodium (p=0.02), while no statistically significant difference was found between total bilirubin (p=0.167), direct bilirubin (p=0.07), uric acid (p=0.16), and potassium (p=0.14).Conclusion. Significantly higher levels of serum VEGF were noted in PIH subjects compared to normal pregnant and control subjects.

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Liang, Songhe, Hao Yu, Xinxin Chen, Tingting Shen, Zhongqi Cui, JunTing Zhang, Yue Cheng et al. « PDGF-BB/KLF4/VEGF Signaling Axis in Pulmonary Artery Endothelial Cell Angiogenesis ». Cellular Physiology and Biochemistry 41, n^o 6 (2017) : 2333–49. http://dx.doi.org/10.1159/000475652.

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Background: Accumulating evidence suggests that platelet-derived growth factor-BB (PDGF-BB) and vascular endothelial growth factor(VEGF) play a role in the progression of pulmonary arterial hypertension (PAH).Since chronic hypoxia is responsible for intimal hyperplasia and disordered angiogenesis of pulmonary arteries, which are histological hallmarks of PAH, we explored the role of the PDGF-BB/KLF4/VEGF signaling axis in the angiogenesis of pulmonary artery endothelial cells (PAECs). Methods: Adult male Wistar rats were used to study hypoxia-induced or monocrotaline (MCT)-induced right ventricular (RV) remodeling as well as systolic function and hemodynamics using echocardiography and a pressure-volume admittance catheter. Morphometric analyses of lung vasculature and RV vessels were performed. Results: The results revealed that both the PDGF receptor-tyrosine kinase inhibitor imatinib and the multi-targeted VEGF and PDGF receptor inhibit or sunitinib malate reversed hypoxia-induced increases in right ventricular systolic pressure (RVSP), right ventricular function and thickening of the medial walls. Mechanistically VEGF/VEGFR and PDGF/PDGFR formed a biological complex. We also showed that PDGF-BBincreasedKLF4 promoter activity transcriptionally activating VEGF expression, which regulates PAEC proliferation; migration; and the cell-cycle transition from G0/G1phase to S phase and G2/M-phase and eventually leads to PAEC angiogenesis Conclusion: Our study indicates that hypoxia-induced angiogenesis of PAECs is associated with increased levels of PDGF-BB/KLF4/VEGF, which contribute to pulmonary vascular remodeling. Overall, our study contributes to a better understanding of PAH pathogenesis.

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Al-Ghazali, Basima, Muna Khadim, Sara Hamza, Hawraa Sahib Al-Haddad, Alaa Salah Jumaah et Najah Hadi. « Identification of vascular endothelial growth factor in preeclampsia in Iraqi women ». Journal of Medicine and Life 15, n^o 10 (octobre 2022) : 1252–56. http://dx.doi.org/10.25122/jml-2021-0211.

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Preeclampsia (PE) is a major obstetric syndrome and represents a pregnancy hypertensive disease affecting about 2–8% of pregnancies. Typically, it occurs after 20 weeks of pregnancy, being classified as early or late in accordance with the gestational age at diagnosis or delivery. An imbalance between angiogenic and antiangiogenic factors has an important role in the pathophysiology of PE. It was hypothesized that the dysfunctional endothelium contributes to the pathogenesis of PE. A change in the production of Vascular endothelial growth factor (VEGR), a biomarker of endothelial dysfunction, is associated with this disease, whether presenting an increase, decrease, or being at a normal level. This study examined the associations between VEGF and preeclampsia and the importance of this VEGF as a predictor of its severity. This case-control study included 50 patients with preeclampsia and 50 normotensive pregnant women in the control group. Venous blood was aspirated from each patient, and VEGF levels were measured from sera. The mean VEGF for patients with mild PE was 29.410±18.976 pg/ml, for those with severe PE it was 36.188±36.98 pg/ml, and for normotensive women it was 92.104±154.715 pg/ml. There were significant differences in VEGF levels between the studied groups (P=0.024). This study showed that serum VEGF levels were significantly reduced in patients with preeclampsia compared with normotensive pregnant women, suggesting marked endothelial dysfunction. This led to widespread vasoconstriction and, in turn, caused hypertension and proteinuria.

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El-Naggar, Abdel Rahman, Dalia Zaafar, Mohammed Elyamany, Soha Hassanin, Atef Bassyouni et Hekma Abdel-Latif. « The Role of Vildagliptin in Treating Hypertension Through Modulating Serum VEGF in Diabetic Hypertensive Patients ». Journal of Cardiovascular Pharmacology and Therapeutics 24, n^o 3 (10 janvier 2019) : 254–61. http://dx.doi.org/10.1177/1074248418817345.

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Background: Several trials have reported that dipeptidyl peptidase-4 (DPP-4) inhibitors are used to improve endothelial function in addition to treating type 2 diabetes (T2DM). The current study investigated the effects of vildagliptin, DPP-4 inhibitor, compared to metformin on endothelial function and blood pressure through vascular endothelial growth factor (VEGF) modulation in patients with T2DM and hypertension. Methods: This study was designed as a randomized controlled parallel study. A total of 120 volunteers were recruited and allocated into 4 groups: healthy volunteers, patients recently diagnosed with hypertension and diabetes, patients treated with captopril for hypertension in addition to metformin, and patients treated with captopril in addition to vildagliptin. The percentage change in body weight was calculated in addition to serum VEGF levels, blood pressure, glycated hemoglobin (HbA1c), total lipid profile, and insulin resistance. Results: At the end of the therapeutic period, the results showed that vildagliptin significantly decreased blood pressure and increased serum VEGF levels, while metformin was more effective at lowering body weight. In comparison with metformin, vildagliptin showed a promising action through its antihypertensive effect via elevating VEGF levels and improving physiological angiogenesis and vasculature. What is new and conclusion: Vildagliptin showed a promising action through its blood pressure-regulating effect via modulating VEGF levels and improving physiological angiogenesis and vasculature, in addition to improving the lipid profile of patients, while metformin was better in reducing body weight.

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Voelkel, Norbert F., R. William Vandivier et Rubin M. Tuder. « Vascular endothelial growth factor in the lung ». American Journal of Physiology-Lung Cellular and Molecular Physiology 290, n^o 2 (février 2006) : L209—L221. http://dx.doi.org/10.1152/ajplung.00185.2005.

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Vascular endothelial growth factor (VEGF) is a pluripotent growth and permeability factor that has a broad impact on endothelial cell function. The lung tissue is very rich in this protein; many different lung cells produce VEGF and also respond to VEGF. VEGF is critical for the development of the lung and serves as a maintenance factor during adult life. In addition to the physiological functions of this protein, there is increasing evidence that VEGF also plays a role in several acute and chronic lung diseases, such as acute lung injury, severe pulmonary hypertension, and emphysema. Here we provide a comprehensive overview of the rapidly expanding literature.

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Lanzl, I., et K. Kotliar. « Können Anti-VEGF-Injektionen Glaukom oder okuläre Hypertension verursachen ? » Klinische Monatsblätter für Augenheilkunde 234, n^o 02 (22 février 2017) : 191–93. http://dx.doi.org/10.1055/s-0043-101819.

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Kruzliak, Peter. « VEGF Pathway Inhibitors-Induced Hypertension : Next Step in Therapy ». Journal of Clinical Hypertension 16, n^o 8 (30 mai 2014) : 617. http://dx.doi.org/10.1111/jch.12348.

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Moreau, Richard. « VEGF-induced angiogenesis drives collateral circulation in portal hypertension ». Journal of Hepatology 43, n^o 1 (juillet 2005) : 6–8. http://dx.doi.org/10.1016/j.jhep.2005.04.002.

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Beaini, Shadia, Youakim Saliba, Joelle Hajal, Viviane Smayra, Jules‐Joel Bakhos, Najat Joubran, Dania Chelala et Nassim Fares. « VEGF‐C attenuates renal damage in salt‐sensitive hypertension ». Journal of Cellular Physiology 234, n^o 6 (30 octobre 2018) : 9616–30. http://dx.doi.org/10.1002/jcp.27648.

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Khorram, Omid, Naseem Khorram, Mazdak Momeni, Guang Han, Jennifer Halem, Mina Desai et Michael G. Ross. « Maternal undernutrition inhibits angiogenesis in the offspring : a potential mechanism of programmed hypertension ». American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, n^o 2 (août 2007) : R745—R753. http://dx.doi.org/10.1152/ajpregu.00131.2007.

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The underlying etiology of many chronic diseases such as hypertension and diabetes has been traced to the in utero environment. Our interest has focused on determining the mechanism of programmed hypertension. In our rodent model of 50% maternal food restriction (MFR) from day 10 of gestation to term, the offspring develop hypertension as adults. We hypothesized that maternal undernutrition inhibits angiogenesis such that the neonate is endowed with fewer microvessels, increasing their susceptibility to develop hypertension as adults. We found significantly reduced number of mesenteric branching and renal medullary microvessels in the 1-day-old MFR newborns. Endothelial cells from MFR offspring generated shorter neovessels in culture compared with controls. The inhibition of angiogenesis was associated with a significant decrease in VEGF protein expression in mesenteric microvessels and aortas in 1-day-old offspring. However, in adulthood there was a marked increase in VEGF expression in both vessel types. The expression of endothelial nitric oxide synthase protein was also found to be increased in both renal and mesenteric microvessels and in aortas in the 1-day-old MFR offspring. These results suggest that MFR results in inhibition of VEGF expression in microvascular and aortic endothelial cells early in life, resulting in decreased angiogenesis and increased peripheral vascular resistance, both of which may contribute to offspring hypertension.

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