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Condition: Hypertension

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Total 587 results found since Jan 2013.

Endothelin-1 decreases endothelial PPAR{gamma} signaling and impairs angiogenesis after chronic intrauterine pulmonary hypertension
Increased endothelin-1 (ET-1) disrupts angiogenesis in persistent pulmonary hypertension of the newborn (PPHN), but pathogenic mechanisms are unclear. Peroxisome proliferator activated receptor (PPAR) is decreased in adult pulmonary hypertension, but whether ET-1-PPAR interactions impair endothelial cell function and angiogenesis in PPHN remains unknown. We hypothesized that increased PPHN pulmonary artery endothelial cell (PAEC) ET-1 production decreases PPAR signaling and impairs tube formation in vitro. Proximal PAECs were harvested from fetal sheep after partial ligation of the ductus arteriosus in utero (PPHN) and con...
Source: AJP: Lung Cellular and Molecular Physiology - February 15, 2014 Category: Respiratory Medicine Authors: Wolf, D., Tseng, N., Seedorf, G., Roe, G., Abman, S. H., Gien, J. Tags: ARTICLES Source Type: research

DOWNREGULATION OF L-TYPE Ca2+ CHANNEL IN RAT MESENTERIC ARTERIES LEADS TO LOSS OF SMOOTH MUSCLE CONTRACTILE PHENOTYPE AND INWARD HYPERTROPHIC REMODELING.
Abstract L-type Ca(2+) channels (LTCCs) are important for vascular smooth muscle cell (VSMC) contraction, as well as VSMC differentiation, as indicated by loss of LTCCs during VSMC dedifferentiation. However it is not clear whether loss of LTCCs is a primary event underlying phenotypic modulation or whether loss of LTCCs has significance for vascular structure. We used small interference RNA transfection in vivo to investigate the role of LTCCs in VSMC phenotypic expression and structure of rat mesenteric arteries. Small interference RNA reduced LTCC mRNA and protein expression in rat mesenteric arteries 3 days af...
Source: American Journal of Physiology. Heart and Circulatory Physiology - February 21, 2014 Category: Physiology Authors: Kudryavtseva O, Møller Herum K, Secher Dam V, Simonsen Straarup M, Kamaev D, Boedtkjer DM, Matchkov VV, Aalkjaer C Tags: Am J Physiol Heart Circ Physiol Source Type: research

Death-associated protein kinase3 mediates vascular structural remodeling via stimulating smooth muscle cell proliferation and migration
Death-associated protein kinase (DAPK)3 also known as zipper-interacting kinase is a serine/threonine kinase that mainly regulates cell death and smooth muscle contraction. We previously found that protein expression of DAPK3 increases in mesenteric artery from spontaneously hypertensive rats (SHR) and that DAPK3 mediates the development of hypertension in SHR partly through promoting reactive oxygen species-dependent vascular inflammation. However, it remains to be clarified how DAPK3 controls smooth muscle cells (SMCs) proliferation and migration that are also important processes for the hypertension development. We ther...
Source: Clinical Science - May 12, 2014 Category: Biomedical Science Authors: T Usui, T Sakatsume, R Nijima, K Otani, K Kazama, T Morita, S Kameshima, M Okada, H Yamawaki Source Type: research

Role of caveolin 1 in AT1a receptor-mediated uptake of angiotensin II in the proximal tubule of the kidney.
Abstract Caveolin 1 (CAV-1) functions not only as a constitutive scaffolding protein of caveolae but also as a vesicular transporter and signaling regulator. In the present study, we tested the hypothesis that CAV-1 knockout (CAV-1 KO) inhibits AT1 (AT1a) receptor-mediated uptake of angiotensin II (ANG II) in the proximal tubule and attenuates blood pressure responses in ANG II-induced hypertension. To determine the role of CAV-1 in mediating the uptake of fluorescein (FITC)-labeled ANG II, wild-type (WT) mouse PT cells (mPCT) were transfected with CAV-1 siRNA for 48 h before AT1a-mediated uptake of FITC-ANG II wa...
Source: Am J Physiol Renal P... - August 27, 2014 Category: Urology & Nephrology Authors: Li XC, Gu V, Miguel-Qin E, Zhuo JL Tags: Am J Physiol Renal Physiol Source Type: research

O13. Catechol-O-methyltransferase deficiency leads to hypersensitivity on the pressor response against angiotensin II
Conclusion Deficiency in COMT and 2-ME are associated with the hypersensitivity on the pressor response against AngII infusion. Similar mechanisms could be relevant to pregnant status and PE.
Source: Pregnancy Hypertension: An International Journal of Womens Cardiovascular Health - August 31, 2015 Category: OBGYN Source Type: research

Dexmedetomidine-Induced Contraction in the Isolated Endothelium-Denuded Rat Aorta Involves PKC-δ-mediated JNK Phosphorylation.
Authors: Yu J, Ok SH, Kim WH, Cho H, Park J, Shin IW, Lee HK, Chung YK, Choi MJ, Kwon SC, Sohn JT Abstract Vasoconstriction mediated by the highly selective alpha-2 adrenoceptor agonist dexmedetomidine leads to transiently increased blood pressure and severe hypertension. The dexmedetomidine-induced contraction involves the protein kinase C (PKC)-mediated pathway. However, the main PKC isoform involved in the dexmedetomidine-induced contraction remains unknown. The goal of this in vitro study was to examine the specific PKC isoform that contributes to the dexmedetomidine-induced contraction in the isolated rat aort...
Source: International Journal of Medical Sciences - September 25, 2015 Category: Biomedical Science Tags: Int J Med Sci Source Type: research

Corin is down-regulated and exerts cardioprotective action via activating pro-atrial natriuretic peptide pathway in diabetic cardiomyopathy
Conclusions: Our results indicate that corin plays an important role in cardioprotection by activating pro-atrial natriuretic peptide pathway in DCM. Corin deficiency leads to endothelial dysfunction and vascular remodeling.
Source: Cardiovascular Diabetology - October 7, 2015 Category: Cardiology Authors: Aiming PangYahui HuPengfei ZhouGuangfeng LongXin TianLi MenYanna ShenYunde LiuYujie Cui Source Type: research

Expression and function of aquaporin 1 in hypoxia-induced pulmonary hypertension
Conclusion: Hx modulates the expression of Aqp1 in vivo and in vitro. Inhibition of Aqp1 through siRNA resulted in less migration and more apoptosis. These data suggest an important functional role of Aqp1 in the development of hypoxia-induced PH.
Source: European Respiratory Journal - October 30, 2015 Category: Respiratory Medicine Authors: Schuoler, C., Haider, T., Leuenberger, C., Gassmann, M., Kohler, M., Huber, L., Brock, M. Tags: 4.3 Pulmonary Circulation and Pulmonary Vascular Disease Source Type: research

Abstract P086: Superoxide but Not Hydrogen Peroxide Increases Nuclear Translocation of Transcription Factor Sp3 and AT1 Receptor Expression in the Renal Cells Session Title: Poster Session 1- Trainee Onsite Poster Competition and Reception
Age-associated oxidative stress causes up-regulation of renal AT1 receptor function (AT1R) and hypertension in aging Fischer Brown Norway (FBN) rats. Here we studied the mechanism of up-regulation of renal AT1R, and further tested superoxide Vs hydrogen peroxide (H2O2) specificity in this phenomenon. We found that transcription factor Sp3 plasmid increased (Control vs Sp3: 0.1165 ± 0.01 vs 0.3810 ± 0.03) while Sp3 siRNA decreased (Control siRNA vs Sp3 siRNA: 1.11 ± 0.25 vs 0.64 ± 0.06) the levels of AT1 receptor protein in human kidney (HK2) cells. Whereas transcription factor NF-kB p-65 plasmid...
Source: Hypertension - November 3, 2015 Category: Cardiology Authors: Saleem, M. Tags: Session Title: Poster Session 1- Trainee Onsite Poster Competition and Reception Source Type: research

Abstract P087: PDI via Keap1/Nrf2 Pathway Regulates Renal AT1 Receptors and Blood Pressure in Aging Rats Session Title: Poster Session 1- Trainee Onsite Poster Competition and Reception
Renal angiotensin AT1 receptor (AT1R) plays pivotal role in the regulation of blood pressure (BP). We recently reported that age-associated oxidative stress causes hyper-activation of AT1R and hypertension in the aging Fischer Brown Norway (FBN) rats. Our objective was to understand the mechanism of higher oxidative stress contributing to the impaired AT1R function in the aged FBNs. Nrf2 transcription factor protects kidney from oxidative stress by activating the transcription of diverse antioxidant and detoxifying enzymes. Kelch-like ECH-associated protein 1 (keap1) inhibit Nrf2 activity by sequestering Nrf2 in cytosol. W...
Source: Hypertension - November 3, 2015 Category: Cardiology Authors: Wang, X., Asghar, M. Tags: Session Title: Poster Session 1- Trainee Onsite Poster Competition and Reception Source Type: research

Abstract 122: Activation of Nuclear Factor Erythroid 2-related Factor 2 (Nrf2) Enhances Cyclooxygenase 2 Expression via Promoter Antioxidant Response Element in Preglomerular Vascular Smooth Muscle Cells (PGVSMCs) Session Title: Concurrent XVIII C: Oxidative Stress II
In conclusion, these results show a novel role of Nrf2 in inducing COX2 expression through binding to promoter ARE in the absence of increased ROS in rat PGVSMCs.
Source: Hypertension - November 3, 2015 Category: Cardiology Authors: Luo, Z., Welch, W. J., Wilcox, C. S. Tags: Session Title: Concurrent XVIII C: Oxidative Stress II Source Type: research

CTRP9 Ameliorates Pulmonary Arterial Hypertension Through Attenuating Inflammation and Improving Endothelial Cell Survival and Function
In conclusion, CTRP9 ameliorated PH by attenuating inflammation and improving endothelial cell survival and function.
Source: Journal of Cardiovascular Pharmacology - May 1, 2016 Category: Cardiology Tags: Original Article Source Type: research

RELM- β promotes human pulmonary artery smooth muscle cell proliferation via FAK-stimulated surviving.
In conclusion, results suggested that FAK is upstream of survivin in the signaling pathway mediating cell proliferation. FAK seems to be important in RELM-β-induced HPASMC proliferation, partially by upregulating survivin expression. PMID: 28041789 [PubMed - as supplied by publisher]
Source: Experimental Cell Research - December 28, 2016 Category: Cytology Authors: Lin C, Li X, Luo Q, Yang H, Li L, Zhou Q, Li Y, Tang H, Wu L Tags: Exp Cell Res Source Type: research

Hypoxia induces arginase II expression and increases viable human pulmonary artery smooth muscle cell numbers via AMPK α1 signaling.
Hypoxia induces arginase II expression and increases viable human pulmonary artery smooth muscle cell numbers via AMPKα1 signaling. Am J Physiol Lung Cell Mol Physiol. 2017 Feb 17;:ajplung.00117.2016 Authors: Xue J, Nelin LD, Chen B Abstract Pulmonary artery smooth muscle cell (PASMC) proliferation is one of the hallmark features of hypoxia-induced pulmonary hypertension. With only supportive treatment options available for this life threatening disease, treating and preventing the proliferation of PASMCs is a viable therapeutic option. A key promoter of hypoxia-induced increases in the number of via...
Source: Am J Physiol Lung Ce... - February 16, 2017 Category: Respiratory Medicine Authors: Xue J, Nelin LD, Chen B Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Hypoxia induces arginase II expression and increases viable human pulmonary artery smooth muscle cell numbers via AMPK{alpha}1 signaling
Pulmonary artery smooth muscle cell (PASMC) proliferation is one of the hallmark features of hypoxia-induced pulmonary hypertension. With only supportive treatment options available for this life-threatening disease, treating and preventing the proliferation of PASMCs is a viable therapeutic option. A key promoter of hypoxia-induced increases in the number of viable human PASMCs is arginase II, with attenuation of viable cell numbers following pharmacologic inhibition or siRNA knockdown of the enzyme. Additionally, increased levels of arginase have been demonstrated in the pulmonary vasculature of patients with pulmonary h...
Source: AJP: Lung Cellular and Molecular Physiology - April 5, 2017 Category: Respiratory Medicine Authors: Xue, J., Nelin, L. D., Chen, B. Tags: RESEARCH ARTICLE Source Type: research