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  • 1
    Online Resource
    Online Resource
    Angiotensin II-induced sudden arrhythmic death and electrical remodeling
    American Physiological Society ; 2007
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 293, No. 2 ( 2007-08), p. H1242-H1253
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 293, No. 2 ( 2007-08), p. H1242-H1253
    Abstract: Rats harboring the human renin and angiotensinogen genes (dTGR) feature angiotensin (ANG) II/hypertension-induced cardiac damage and die suddenly between wk 7 and 8. We observed by electrocardiogram (ECG) telemetry that ventricular tachycardia (VT) is a common terminal event in these animals. Our aim was to investigate electrical remodeling. We used ECG telemetry, noninvasive cardiac magnetic field mapping (CMFM) at wk 5 and 7, and performed in vivo programmed electrical stimulation at wk 7. We also investigated whether or not losartan (Los; 30 mg·kg −1 ·day −1 ) would prevent electrical remodeling. Cardiac hypertrophy and systolic blood pressure progressively increased in dTGR compared with Sprague-Dawley (SD) controls. Already by wk 5, untreated dTGR showed increased perivascular and interstitial fibrosis, connective tissue growth factor expression, and monocyte infiltration compared with SD rats, differences that progressed through time. Left-ventricular mRNA expression of potassium channel subunit Kv4.3 and gap-junction protein connexin 43 were significantly reduced in dTGR compared with Los-treated dTGR and SD. CMFM showed that depolarization and repolarization were prolonged and inhomogeneous. Los ameliorated all disturbances. VT could be induced in 88% of dTGR but only in 33% of Los-treated dTGR and could not be induced in SD. Untreated dTGR show electrical remodeling and probably die from VT. Los treatment reduces myocardial remodeling and predisposition to arrhythmias. ANG II target organ damage induces VT.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.01400.2006
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2007
    detail.hit.zdb_id: 1477308-9
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  • 2
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    Bcl10 Mediates Angiotensin II–Induced Cardiac Damage and Electrical Remodeling
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Hypertension Vol. 64, No. 5 ( 2014-11), p. 1032-1039
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 64, No. 5 ( 2014-11), p. 1032-1039
    Abstract: Angiotensin (Ang) II is a potent mediator of both hypertension and cardiac damage; however, the mechanisms by which this occur remain unclear. B-cell lymphoma/leukemia 10 (Bcl10) is a member of the CBM signalosome, which links Ang II and nuclear factor-κB signaling. We hypothesized that Bcl10 is pivotal in the pathogenesis of Ang II–induced cardiac damage. Ang II infusion in mice lacking Bcl10 resulted in reduced cardiac fibrosis, less cellular infiltration, and improved arrhythmogenic electric remodeling, despite a similar degree of hypertension or cardiac hypertrophy. Adoptive transfer of bone marrow (BM), whereby Bcl10 knockout or wildtype BM was transferred to their opposite genotype recipients, revealed the dual importance of Bcl10 within both cardiac and immune cells. Loss of Bcl10 in cardiac cells resulted in reduced expression of genes important for the adhesion and recruitment of immune cells. In vitro experiments demonstrated that adhesion of monocytes to Ang II–treated endothelial cells also required Bcl10. Additionally, Bcl10 deficiency in macrophages reduced their intrinsic migratory ability. To address the role of BM-derived fibroblasts in the formation of cardiac fibrosis, we explored whether Bcl10 is also important for the infiltration of BM-derived (myo)fibroblasts into the heart. The transfer of green fluorescent protein positive wildtype BM into Bcl10 knockout recipient mice revealed a reduced number of noncardiac (myo)fibroblasts compared with those wildtype recipients. Our results demonstrate the significant role of Bcl10 in multiple cell types important for the generation of Ang II–induced cardiac damage and electric remodeling and may provide a new avenue for therapeutic intervention.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.114.03900
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 2094210-2
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  • 3
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    Angiotensin II Type 1 Receptor Antibodies and Increased Angiotensin II Sensitivity in Pregnant Rats
    Ovid Technologies (Wolters Kluwer Health) ; 2011
    In:  Hypertension Vol. 58, No. 1 ( 2011-07), p. 77-84
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 58, No. 1 ( 2011-07), p. 77-84
    Abstract: Pregnant women who subsequently develop preeclampsia are highly sensitive to infused angiotensin (Ang) II; the sensitivity persists postpartum. Activating autoantibodies against the Ang II type 1 (AT 1 ) receptor are present in preeclampsia. In vitro and in vivo data suggest that they could be involved in the disease process. We generated and purified activating antibodies against the AT 1 receptor (AT 1 -AB) by immunizing rabbits against the AFHYESQ epitope of the second extracellular loop, which is the binding epitope of endogenous activating autoantibodies against AT 1 from patients with preeclampsia. We then purified AT 1 -AB using affinity chromatography with the AFHYESQ peptide. We were able to detect AT 1 -AB both by ELISA and a functional bioassay. We then passively transferred AT 1 -AB into pregnant rats, alone or combined with Ang II. AT 1 -AB activated protein kinase C-α and extracellular-related kinase 1/2. Passive transfer of AT 1 -AB alone or Ang II (435 ng/kg per minute) infused alone did not induce a preeclampsia-like syndrome in pregnant rats. However, the combination (AT 1 -AB plus Ang II) induced hypertension, proteinuria, intrauterine growth retardation, and arteriolosclerosis in the uteroplacental unit. We next performed gene-array profiling of the uteroplacental unit and found that hypoxia-inducible factor 1α was upregulated by Ang II plus AT 1 -AB, which we then confirmed by Western blotting in villous explants. Furthermore, endothelin 1 was upregulated in endothelial cells by Ang II plus AT 1 -AB. We show that AT 1 -AB induces Ang II sensitivity. Our mechanistic study supports the existence of an “autoimmune-activating receptor” that could contribute to Ang II sensitivity and possible to preeclampsia.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.111.171348
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2011
    detail.hit.zdb_id: 2094210-2
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  • 4
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    Online Resource
    Energy Metabolism in Human Renin-Gene Transgenic Rats : Does Renin Contribute to Obesity?
    Ovid Technologies (Wolters Kluwer Health) ; 2009
    In:  Hypertension Vol. 53, No. 3 ( 2009-03), p. 516-523
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 53, No. 3 ( 2009-03), p. 516-523
    Abstract: Renin initiates angiotensin II formation and has no other known functions. We observed that transgenic rats (TGR) overexpressing the human renin gene (hREN) developed moderate obesity with increased body fat mass and glucose intolerance compared with nontransgenic Sprague-Dawley (SD) rats. The metabolic changes were not reversed by an angiotensin-converting enzyme inhibitor, a direct renin inhibitor, or by (pro)renin receptor blocker treatment. The obese phenotype in TGR(hREN) originated from higher food intake, which was partly compensated by increases in resting energy expenditure, total thermogenesis (postprandial and exercise activity), and lipid oxidation during the first 8 weeks of life. Once established, the difference in body weight between TGR(hREN) and SD rats remained constant over time. When restricted to the caloric intake of SD, TGR(hREN) developed an even lower body weight than nontransgenic controls. We did not observe significant changes in the cocaine and amphetamine-regulated transcript, pro-opiomelanocortin, both anorexigenic, or neuropeptide Y, orexigenic, mRNA levels in TGR(hREN) versus SD controls. However, the mRNA level of the agouti-related peptide, orexigenic, was significantly reduced in TGR(hREN) versus SD controls at the end of the study, which indicates a compensatory mechanism. We suggest that the human renin transgene initiates a process leading to increased and early appetite, obesity, and metabolic changes not related to angiotensin II. The mechanisms are independent of any currently known renin-related effects.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.108.124966
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2009
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  • 5
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    Vascular Endothelial Cell–Specific NF-κB Suppression Attenuates Hypertension-Induced Renal Damage
    Ovid Technologies (Wolters Kluwer Health) ; 2007
    In:  Circulation Research Vol. 101, No. 3 ( 2007-08-03), p. 268-276
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 101, No. 3 ( 2007-08-03), p. 268-276
    Abstract: Nuclear factor kappa B (NF-κB) participates in hypertension-induced vascular and target-organ damage. We tested whether or not endothelial cell–specific NF-κB suppression would be ameliorative. We generated Cre/lox transgenic mice with endothelial cell–restricted NF-κB super-repressor IκBαΔN (Tie-1-ΔN mice) overexpression. We confirmed cell-specific IκBαΔN expression and reduced NF-κB activity after TNF-α stimulation in primary endothelial cell culture. To induce hypertension with target-organ damage, we fed mice a high-salt diet and N(omega)-nitro- l -arginine-methyl-ester (L-NAME) and infused angiotensin (Ang) II. This treatment caused a 40-mm Hg blood pressure increase in both Tie-1-ΔN and control mice. In contrast to control mice, Tie-1-ΔN mice developed a milder renal injury, reduced inflammation, and less albuminuria. RT-PCR showed significantly reduced expression of the NF-κB targets VCAM-1 and ICAM-1, compared with control mice. Thus, the data demonstrate a causal link between endothelial NF-κB activation and hypertension-induced renal damage. We conclude that in vivo NF-κB suppression in endothelial cells stops a signaling cascade leading to reduced hypertension-induced renal damage despite high blood pressure.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.107.150474
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2007
    detail.hit.zdb_id: 1467838-X
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  • 6
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    Abstract 458: Relaxin Did Not Improve Angiotensin II-induced Target Organ Damage
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Hypertension Vol. 62, No. suppl_1 ( 2013-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 62, No. suppl_1 ( 2013-09)
    Abstract: We investigated whether or not Relaxin ameliorates the hypertension induced damage to heart and kidney. We used double transgenic rats harboring both human renin and angiotensinogen genes (dTGRs). These rats develop moderately severe Hypertension but die of end-organ cardiac and renal damage by week 7. Untreated dTGRs had an around 50% mortality rate at 7 weeks. The heart shows necrosis and fibrosis, whereas the kidneys esemble the hemolytic-uremic syndrome vasculopathy. We started Relaxin-treatment on four weeks old dTGR in low (26 μg/kg/d) and high dose (240 μg/kg/d) and age-matched SD rats. Blood-pressure- and albuminuria-measurements were monitored during the treatment period (three weeks). Seven weeks old animals were killed, hearts and kidneys were isolated and used for histochemical and quantitative TaqMan RT-PCR analysis. Systolic blood pressure increased progressively in untreated dTGRs from 161.6 ± 3.02 mmHg in week 5 to 225.3 ± 4.48 mmHg in week 7. Relaxin treatment had no significant influence on blood pressure (low dose 208.0 ± 5.51 mmHg and high dose 222.2 ± 5.60 mmHg at week 7 ) whereas SD rats were normotensive (106.3 ± 1.15 mmHg). Untreated (5.38 ± 0.13 mg/g) and Relaxin treated dTGRs (low dose 5.20 ± 0.18 mg/g and high dose 5.33 ± 0.29 mg/g) had similar cardiac hypertrophy indices (heart-to-body weight ratio), which were significantly higher compared with nontransgenic SD rats (2.90 ± 0.08 mg/g). BNP and CTFG mRNA expression in the hearts was significant higher in untreated dTGRs compared to SD rats. There were no differences in BNP and CTFG expression between untreated and Relaxin treated dTGRs. Relaxin treatment (low dose 78502 ± 16848 μg/day and high dose 43642 ± 10852 μg/day at week 7) did not ameliorate albuminuria compared with untreated dTGRs (57937 ± 6122 μg/day at week 7). Furthermore the treatment with Relaxin did not prevent matrix deposition in the heart and kidney of d TGRs. Finally, Relaxin treatment did not reduce mortality. Although survival was 52 %, in untreated dTGRs 36 % in low dose and 54 % high dose Relaxin treated dTGRs at week 7. These data demonstrate that Relaxin did not improve angiotensin II-induced target organ damage.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.62.suppl_1.A458
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
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  • 7
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    Abstract 459: Vasoactivity of the Alzheimer ß-Amyloid Peptides is Mediated by an Activation of the a 1 -Adrenoreceptor
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Hypertension Vol. 62, No. suppl_1 ( 2013-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 62, No. suppl_1 ( 2013-09)
    Abstract: Alzheimer disease (AD) features β-amyloid peptide (Aβ) deposition in brain and blood vessels and is associated with hypertension. Aβ can cause vasoconstriction and endothelial dysfunction. Recently, we could show that Aβ peptides elicit a signal transduction pathway in vascular smooth muscle cells and cardiomyocytes, induced by α 1 -adrenergic receptor activation. We hypothesized that the Aβ vasoactivity is also induced by activation of the α 1 -adrenoreceptor. Mouse aortic Rings were incubated for 24 h with 1 μmol/l Aβ (25-35). The influence of Aβ (25-35) on vasoconstriction of mouse aortic rings was studied in the additional presence and absence of α 1 -adrenergic receptor blocker prazosin. Vasoactivity in isolated aortic rings was measured using an isometric myograph. Vasoconstriction to 5-hydroxytryptamine was significantly increased (P≤0.001) in aortic rings by Aβ (25-35) pretreatment. This vasoactive effect was improved by the presence of α 1 -adrenergic receptor blocker during the Aβ (25-35) pretreatment. Rat middle cerebral artery (MCA) segments were treated with either 0.1μmol/L Aβ (25-35) or 0.1μmol/L of a negative control peptide with a reverse amino acid sequence (Aβ rev.) of Aβ (25-35) for 4h. Constriction of the middle cerebral artery was measured in dual vessel chamber. Incubation with Aβ (25-35) significantly enhanced (P≤0.0005) response of middle cerebral artery segments to the α 1 -agonist phenylephrine induced contractions. In a further ex vivo model of Langendorff-perfused rat hearts Aβ (25-35) also induced vasoconstriction of coronary arteries that resulted in decreased coronary flow. These effects could also be reversed by α 1 -adrenergic receptor blockade. Furthermore we analyzed the brain of hypertensive dTGR animals and in human arteriosclerotic plaques for the presence of Aβ amyloid. Amyloid deposits are present in cerebral cortex of hypertensive dTGR animals with damaged blood-brain barrier and in human arteriosclerotic plaques. Our data are relevant to the association between AD and hypertension. They may serve to explain impaired of vascular responses by Aβ and could have therapeutic implications.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.62.suppl_1.A459
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
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  • 8
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    Online Resource
    Interferon-γ Signaling Inhibition Ameliorates Angiotensin II–Induced Cardiac Damage
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Hypertension Vol. 60, No. 6 ( 2012-12), p. 1430-1436
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 60, No. 6 ( 2012-12), p. 1430-1436
    Abstract: Angiotensin (Ang) II induces vascular injury in part by activating innate and adaptive immunity; however, the mechanisms are unclear. We investigated the role of interferon (IFN)-γ and interleukin (IL)-23 signaling. We infused Ang II into IFN-γ receptor (IFN-γR) knockout mice and wild-type controls, as well as into mice treated with neutralizing antibodies against IL-23 receptor and IL-17A. Ang II–treated IFN-γR knockout mice exhibited reduced cardiac hypertrophy, reduced cardiac macrophage and T-cell infiltration, less fibrosis, and less arrhythmogenic electric remodeling independent of blood pressure changes. In contrast, IL-23 receptor antibody treatment did not reduce cardiac hypertrophy, fibrosis, or electric remodeling despite mildly reduced inflammation. IL-17A antibody treatment behaved similarly. In the kidney, IFN-γR deficiency reduced inflammation and tubulointerstitial damage and improved glomerular filtration rate. Nonetheless, albuminuria was increased compared with Ang II–treated wild-type controls. The glomeruli of Ang II–treated IFN-γR knockout mice exhibited fewer podocytes, less nephrin and synaptopodin staining, and impaired podocyte autophagy. Thus, IFN-γ blockade, but not IL-23 receptor antibody treatment, protects from Ang II–induced cardiac damage and electric remodeling. In the kidney, IFN-γ signaling acts in a cell type–specific manner. Glomerular filtration rate is preserved in the absence of the IFN-γR, whereas podocytes may require the IFN-γR in the presence of Ang II for normal integrity and function.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.112.199265
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 2094210-2
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  • 9
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    Amyloid-β Peptides Activate α 1 -Adrenergic Cardiovascular Receptors
    Ovid Technologies (Wolters Kluwer Health) ; 2013
    In:  Hypertension Vol. 62, No. 5 ( 2013-11), p. 966-972
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 62, No. 5 ( 2013-11), p. 966-972
    Abstract: Alzheimer disease features amyloid-β (Aβ) peptide deposition in brain and blood vessels and is associated with hypertension. Aβ peptide can cause vasoconstriction and endothelial dysfunction. We observed that Aβ peptides exert a chronotropic effect in neonatal cardiomyocytes, similar to α 1 -adrenergic receptor autoantibodies that we described earlier. Recently, it was shown that α 1 -adrenergic receptor could impair blood–brain flow. We hypothesized that Aβ peptides might elicit a signal transduction pathway in vascular cells, induced by α 1 -adrenergic receptor activation. Aβ (25–35) and Aβ (10–35) induced a positive chronotropic effect in the cardiac contraction assay (28.75±1.15 and 29.40±0.98 bpm), which was attenuated by α 1 -adrenergic receptor blockers (urapidil, 1.53±1.17 bpm; prazosin, 0.30±0.96 bpm). Both Aβ peptides induced an intracellular calcium release in vascular smooth muscle cells. Chronotropic activity and calcium response elicited by Aβ (25–35) were blocked with peptides corresponding to the first extracellular loop of the α 1 -adrenergic receptor. We observed an induction of extracellular-regulated kinase 1/2 phosphorylation by Aβ (25–35) in Chinese hamster ovary cells overexpressing α 1 -adrenergic receptor, vascular smooth muscle cells, and cardiomyocytes. We generated an activation-state–sensitive α 1 -adrenergic receptor antibody and visualized activation of the α 1 -adrenergic receptor by Aβ peptide. Aβ (25–35) induced vasoconstriction of mouse aortic rings and in coronary arteries in Langendorff-perfused rat hearts that resulted in decreased coronary flow. Both effects could be reversed by α 1 -adrenergic receptor blockade. Our data are relevant to the association between Alzheimer disease and hypertension. They may explain impairment of vascular responses by Aβ and could have therapeutic implications.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.113.01348
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2013
    detail.hit.zdb_id: 2094210-2
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  • 10
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    Dietary n-3 Polyunsaturated Fatty Acids and Direct Renin Inhibition Improve Electrical Remodeling in a Model of High Human Renin Hypertension
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Hypertension Vol. 51, No. 2 ( 2008-02), p. 540-546
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 51, No. 2 ( 2008-02), p. 540-546
    Abstract: We compared the effect n-3 polyunsaturated fatty acids (PUFAs) with direct renin inhibition on electrophysiological remodeling in angiotensin II–induced cardiac injury. We treated double-transgenic rats expressing the human renin and angiotensinogen genes (dTGRs) from week 4 to 7 with n-3 PUFA ethyl-esters (Omacor; 25-g/kg diet) or a direct renin inhibitor (aliskiren; 3 mg/kg per day). Sprague-Dawley rats were controls. We performed electrocardiographic, magnetocardiographic, and programmed electrical stimulation. Dietary n-3 PUFAs increased the cardiac content of eicosapentaenoic and docosahexaenoic acid. At week 7, mortality in dTGRs was 31%, whereas none of the n-3 PUFA- or aliskiren-treated dTGRs died. Systolic blood pressure was modestly reduced in n-3 PUFA-treated (180±3 mm Hg) compared with dTGRs (208±5 mm Hg). Aliskiren-treated dTGRs and Sprague-Dawley rats were normotensive (110±3 and 119±6 mm Hg, respectively). Both n-3 PUFA–treated and untreated dTGRs showed cardiac hypertrophy and increased atrial natriuretic peptide levels. Prolonged QRS and QT c intervals and increased T-wave dispersion in dTGRs were reduced by n-3 PUFAs or aliskiren. Both treatments reduced arrhythmia induction from 75% in dTGRs to 17% versus 0% in Sprague-Dawley rats. Macrophage infiltration and fibrosis were reduced by n-3 PUFAs and aliskiren. Connexin 43, a mediator of intermyocyte conduction, was redistributed to the lateral cell membranes in dTGRs. n-3 PUFAs and aliskiren restored normal localization to the intercalated disks. Thus, n-3 PUFAs and aliskiren improved electrical remodeling, arrhythmia induction, and connexin 43 expression, despite a 70-mm Hg difference in blood pressure and the development of cardiac hypertrophy.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.107.103143
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
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