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  • 1
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    Aldosterone, mineralocorticoid receptors, and vascular inflammation
    Ovid Technologies (Wolters Kluwer Health) ; 2007
    In:  Current Opinion in Internal Medicine Vol. 6, No. 3 ( 2007-06), p. 295-303
    Details
    In: Current Opinion in Internal Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 6, No. 3 ( 2007-06), p. 295-303
    Type of Medium: Online Resource
    ISSN: 1535-5942
    URL: Article
    DOI: 10.1097/MNH.0b013e32801245bb
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2007
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  • 2
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    Immune-related effects in hypertension and target-organ damage
    Ovid Technologies (Wolters Kluwer Health) ; 2011
    In:  Current Opinion in Nephrology & Hypertension Vol. 20, No. 2 ( 2011-03), p. 113-117
    Details
    In: Current Opinion in Nephrology & Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 20, No. 2 ( 2011-03), p. 113-117
    Type of Medium: Online Resource
    ISSN: 1062-4821
    URL: Article
    DOI: 10.1097/MNH.0b013e3283436f88
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2011
    detail.hit.zdb_id: 2029133-4
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  • 3
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    1085-195 The renin inhibitor aliskiren is a potent and long-acting antihypertensive in double transgenic rats expressing human renin and angiotensinogen genes
    Elsevier BV ; 2004
    In:  Journal of the American College of Cardiology Vol. 43, No. 5 ( 2004-03), p. A483-
    Details
    In: Journal of the American College of Cardiology, Elsevier BV, Vol. 43, No. 5 ( 2004-03), p. A483-
    Type of Medium: Online Resource
    ISSN: 0735-1097
    URL: Article
    DOI: 10.1016/S0735-1097(04)92043-8
    RVK:
    XA 17760
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2004
    detail.hit.zdb_id: 1468327-1
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  • 4
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    Cytochrome P450 Isoform Expression in Human Vascular Endothelial Cells
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Hypertension Vol. 36, No. suppl_1 ( 2000-10), p. 698-698
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 36, No. suppl_1 ( 2000-10), p. 698-698
    Abstract: P29 Epoxy derivatives of arachidonic acid may act as important autocrine and paracrine mediators of endothelial function including regulation of vascular tone and control of inflammation. To identify potential candidates for catalyzing the synthesis of these and further arachidonic acid metabolites, we studied human vascular endothelial cells for the expression of individual cytochrome P450 isoforms belonging to the CYP families 1, 2, 3 and 4. An RT-PCR screening performed with subfamily- and isoform-specific primer pairs revealed mRNAs for the P450 forms 1A1, 1B1, 2C8, 2E1, 2J2, 3A7, 4A11 and 4F2. The identity of the RT-PCR products was confirmed by DNA sequencing. In addition, P450 1A2 mRNA was detected after induction with β-naphthoflavone which also enhanced the expresion of P450s 1A1 and 1B1. P450s 2B6 and 3A4 were not detectable. Similar P450 isoform patterns were obtained analyzing primary human endothelial cells originating from aorta, coronary arteries, dermal microvessels and umbilical veins, as well as an immortalized human endothelial cell line (HMEC-1). Further studies with HMEC-1 cells showed the expression of all human members of the P450 2C subfamily (2C8, 2C9, 2C18 and 2C19). We next used gaschromatography-mass spectrometry to identify the regioisomeric epoxeicosatrienoic acids produced by HMEC-1 cells. Among the P450 forms detected by the RT-PCR screening, P450 2C8 and 2J2 are the leading candidates for producing vasoactive epoxyeicosatrienoic acids. Using recombinant human P450 1A1, we then found that this P450 form catalyzes the formation of various regioisomeric hydroxy derivatives of arachidonic acid. We conclude that P450 1A1 known primarily for its role in polycyclic aromatic hydrocarbon metabolism, may interfere with endothelial arachidonic acid metabolism, particularly after its induction by drugs and xenobiotics. Furthermore, P450s 4A11 and 4F2 probably contribute to the degradation of lipid mediators of inflammation.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.36.suppl_1.698-a
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
    detail.hit.zdb_id: 2094210-2
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  • 5
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    Abstract 504: 23Na Magnetic Resonance Imaging-Determined Tissue Sodium Increases With Age.
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Hypertension Vol. 60, No. suppl_1 ( 2012-09)
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 60, No. suppl_1 ( 2012-09)
    Abstract: Hypertension is the most common cardiovascular risk factor and systolic blood pressure increases continuously with age. Increased vascular stiffness, nitric oxide, renin-angiotensin aldosterone system and salt intake have been implicated. We have developed 23 Na magnetic resonance imaging ( 23 Na MRI) and showed that aldosterone influences tissue Na + storage. We reasoned that Na + might accumulate in tissues with age. We investigated tissue Na + of the lower leg in 113 subjects with 3T 23 Na MRI. Tissue Na + concentration was calibrated by solutions containing 10 to 40 mmol/l of Na + . Prior to 23 Na MRI measurements, a medical history was taken, blood and urine samples were obtained and blood pressure was analyzed in seated position. The age of the 113 subjects analyzed by 23 Na MRI ranged from 22 to 90 years. We studied 44 women and 69 men. Hypertension was diagnosed in 46 subjects (29 men and 17 women). Men showed an exponential increase in tissue Na + with age (muscle R 2 = 0.54, skin R 2 = 0.33). In contrast, tissue Na + in women was only slightly affected by age and increased linearly (skin R 2 = 0.40, muscle R 2 = 0.13). To compare subpopulations, we allocated the participants into three different age groups 〈 50, 50-65 and 〉 65 years. A gender difference in skin tissue Na + could be found throughout all groups with higher levels in men (14.3 vs. 18.1 ( 〈 50 yrs), 19.0 vs. 24.5 (50-65 yrs), 20.1 vs. 27.4 mmol/l ( 〉 65 yrs); p 〈 0.05). Skin Na + content was elevated in hypertensive women compared to age-matched controls (17.2, n = 12 vs. 21.0 mmol/l, n = 17; p 〈 0.05). We could not identify such a difference in hypertensive versus normotensive men. In line with our previous results, older hypertensive patients receiving an aldosterone antagonist revealed muscle Na + values below age-matched subjects (17.6, n = 6 vs. 21.3 mmol/l, n = 24; p 〈 0.05). We conclude that aging is associated with Na + tissue accumulation with a pronounced gender difference. Skin Na + overload occurs in hypertensive women but not in men. Aldosterone antagonists may reset the age-dependent muscle Na + overload to levels of young healthy controls.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.60.suppl_1.A504
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 2094210-2
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  • 6
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    Angiotensin II Promotes Anti-Apoptosis Via Akt-Kinase Phosphorylation, an Effect Ameliorated by High Dose Aspirin
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Hypertension Vol. 36, No. suppl_1 ( 2000-10), p. 679-680
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 36, No. suppl_1 ( 2000-10), p. 679-680
    Abstract: 11 The balance between cell proliferation and apoptosis is essential for physiological function. We tested the hypothesis that angiotensin II (ANG II) has anti-apoptotic effects via the activation of AKT kinase in rats overexpressing the human renin and angiotensinogen genes (dTGR). dTGR are hypertensive (182±8 mm Hg) with severe renal damage (150-fold increased albuminuria), perivascular and interstitial fibrosis and vasculopathy, and die at 7 weeks. Renal NF-κB DNA binding activity is increased. We studied the time course of the pathogenesis from week 5 to week 7. Blood pressure, albuminuria, fibrosis, vasculopathy and monocyte infiltration increased over time. In contrast, KI-67 proliferating cells were more abundant in week 5 compared to week 7 as well as compared to non-transgenic rats. Phosphorylation of AKT kinase increased with the severity of the disease. Immunostaining of p-AKT and the activated NF-κB subunit p65 were observed in the glomeruli and endothelium. While Bcl-2 and phosphorylated Bad was predominantly expressed in the endothelium in week 7, the strongest bax immunostaining in the vessel wall media was observed in week 5. We then investigated the effect of chronic high dose aspirin (ASA; 600 mg/kg/d) on remodeling. While ASA did not change blood pressure, albuminuria and fibrosis were similar to non-transgenic controls. ASA completely normalized AKT protein synthesis as well as AKT phosphorylation and NF-κB DNA binding activity. Bax immunostaining at week 7 increased in the media, while Bcl-2 decreased. Western blot in dTGR kidney homogenates showed increased Bcl-2 levels compared ASA-treated and non-transgenic rats. We then confirmed the effect of ASA on p-AKT stimulating endothelial cells in vitro with ANG II (10-7 M; 10 min). Western blot showed reduced p-AKT in ASA pretreated cells. These results show that ANG II is anti-apoptotic by activating AKT kinase. ASA is able to restore the impaired balance of tissue remodeling. Finally, in addition to inhibiting I-κB kinase, ASA may exert a part of its ameliorating effects in this model by inhibiting AKT phosphorylation.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.36.suppl_1.679-a
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
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  • 7
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    Cardiac Protective Effect of Aldosterone Blockade Is Mediated Through Ap-1 and Nf-κB Suppression in Angiotensin Ii-Induced Cardiac Damage
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Hypertension Vol. 36, No. suppl_1 ( 2000-10), p. 691-692
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 36, No. suppl_1 ( 2000-10), p. 691-692
    Abstract: 77 Aldosterone is a multifunctional mineralocorticoid affecting homeostasis of water and electrolytes, sympathetic activity, and tissue fibrosis. Aldosterone synthesis is induced by activation of the renin-angiotensin system. We tested whether or not the inhibition of aldosterone signaling can prevent fibrotic tissue remodeling in vivo. In a transgenic rat model overexpressing the human renin and angiotensinogen gens (dTGR), we investigated the effect of spironolactone (SPIRO 20 mg/kg/d) and the AT1 receptor blocker valsartan (VAL; 10 mg/kg/d) on growth factors and transcription factors leading chronic inflammation and tissue fibrosis. Untreated dTGR develop severe hypertension, cardiac hypertrophy, vasculopathy, and perivascular fibrosis. The hearts also show chronic inflammation and the animals have a 50% mortality at 7 weeks. VAL completely reversed these pathological features. SPIRO and VAL both prevented mortality, while only VAL normalized systolic blood pressure (VAL 121±9, SPIRO 161±11, dTGR 182±8, SD 109±2 mm Hg). Both reduced cardiac hypertrophy (SPIRO 4.2±0.1, VAL 3.6±0.1, dTGR 5.7±0.2, SD 3.6±0.1 mg/g) and reduced vasculopathy. Quantitative bFGF RT-PCR showed a complete mRNA reduction in the left ventricle in both treatment groups (SPIRO 11±4, VAL 5±1 dTGR 43±4, SD 4±1 arbitrary units). In contrast, RT-PCR of TGF beta and PDGF showed no upregulation in dTGR compared to non-transgenic hearts. Gel shift assay of the heart demonstrated a suppression of AP-1 and NF-κB DNA binding activity after SPIRO and VAL treatment. Immunohistology revealed reduced bFGF expression and less collagen I, fibronectin, and laminin in the interstitium of SPIRO and VAL-treated rats. These findings show that aldosterone promotes hypertrophy, cardiac remodeling, and fibrosis. In dTGR hearts this effect is at least partly mediated through the transcription factors AP-1 and NF-κB as well as bFGF. Blocking the aldosterone receptor downregulates these effector molecules and reduces angiotensin II-induced cardiac damage.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.36.suppl_1.691-e
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
    detail.hit.zdb_id: 2094210-2
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  • 8
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    Angiotensin II induced inflammation in the kidney and in the heart of double transgenic rats
    Springer Science and Business Media LLC ; 2001
    In:  BMC News and views Vol. 1, No. S2 ( 2001-12)
    Details
    In: BMC News and views, Springer Science and Business Media LLC, Vol. 1, No. S2 ( 2001-12)
    Type of Medium: Online Resource
    ISSN: 1471-8219
    URL: Article
    DOI: 10.1186/2048-4623-1-S2-054
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2001
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  • 9
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    Levosimendan improves cardiac function and survival in rats with angiotensin II-induced hypertensive heart failure
    Springer Science and Business Media LLC ; 2010
    In:  Hypertension Research Vol. 33, No. 10 ( 2010-10), p. 1004-1011
    Details
    In: Hypertension Research, Springer Science and Business Media LLC, Vol. 33, No. 10 ( 2010-10), p. 1004-1011
    Type of Medium: Online Resource
    ISSN: 0916-9636 , 1348-4214
    URL: Article
    DOI: 10.1038/hr.2010.123
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2010
    detail.hit.zdb_id: 2110941-2
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  • 10
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    Renal and Mesenteric Arterial Tone in Rats with Human Renin and Angiotensinogen Genes
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Hypertension Vol. 36, No. suppl_1 ( 2000-10), p. 694-694
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 36, No. suppl_1 ( 2000-10), p. 694-694
    Abstract: P6 The vascular endothelium plays a key role in the control of vasomotor tone, local hemostasis, and vascular wall proliferation processes. We characterized vascular functions in double-transgenic rats (dTGR) harboring human renin and human angiotensinogen. In dTGR, the endothelium-mediated relaxations of noradrenaline (NA)-precontracted renal (large conduit vessel) and mesenteric arterial (smaller conduit vessel) rings to acetylcholine (ACh) were markedly impaired, compared to normotensive Sprague Dawley rats (p 〈 0.05). In contrast, the endothelium-independent relaxation to sodium nitroprusside (SNP) were similar in both strains. Preincubation of the arterial rings with the NOS inhibitor L-NAME and the COX inhibitor diclofenac inhibited relaxations to ACh almost completely in dTGR, suggesting that endothelial dysfunction could be attributed, at least in part, to reduced relaxation via arterial K+ channels. Contractions to Ang II, ET-1, and NA were decreased in dTGR suggesting agonist-dependent down-regulation of the receptors. The vascular media-to-lumen ratio was similar in both strains, indicating that vascular functions were characterized during an early stage of hypertension. 24-hour urinary NOx excretion, a marker of total body NO generation, was markedly decreased in dTGR (p 〈 0.05). AT1 receptor blockade by valsartan (30 mg/kg p.o. for 3 weeks) normalized blood pressure, endothelial dysfunction, and the contractile responses to ET-1 and NA. We also quantified AT1, AT2, neutral endopeptidase (NEP), and ACE expressions in the kidney by autoradiography. In dTGR, AT1, AT2 and NEP expressions were decreased, whereas ACE expression was unchanged. The activity of renal xanthine oxidoreductase (XOR), a hypoxia-inducible enzyme capable of generating reactive oxygen species, was increased by 50 % in dTGR, and normalized by valsartan. Our findings indicate that hypertension in dTGR is associated with endothelial dysfunction, down-regulation of Ang II, ET-1, and NA receptors, as well as increased renal XOR activity. AT1 receptor blockade effectively normalized blood pressure, alterations in arterial function, and renal XOR activity.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/hyp.36.suppl_1.694-a
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
    detail.hit.zdb_id: 2094210-2
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