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  • 1
    Online Resource
    Online Resource
    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
    detail.hit.zdb_id: 2094210-2
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  • 2
    Online Resource
    Online Resource
    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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  • 3
    Online Resource
    Online Resource
    Vitamin D Depletion Aggravates Hypertension and Target‐Organ Damage
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Journal of the American Heart Association Vol. 4, No. 2 ( 2015-01-30)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 4, No. 2 ( 2015-01-30)
    Abstract: We tested the controversial hypothesis that vitamin D depletion aggravates hypertension and target‐organ damage by influencing renin. Methods and Results Four‐week‐old double‐transgenic rats ( dTGR ) with excess angiotensin (Ang) II production due to overexpression of the human renin ( hREN ) and angiotensinogen ( hAGT ) genes received vitamin D‐depleted (n=18) or standard chow (n=15) for 3 weeks. The depleted group had very low serum 25‐hydroxyvitamin D levels (mean± SEM ; 3.8±0.29 versus 40.6±1.19 nmol/L) and had higher mean systolic BP at week 5 (158±3.5 versus 134.6±3.7 mm Hg, P 〈 0.001), week 6 (176.6±3.3 versus 162.3±3.8 mm Hg, P 〈 0.01), and week 7 (171.6±5.1 versus 155.9±4.3 mm Hg, P 〈 0.05). Vitamin D depletion led to increased relative heart weights and increased serum creatinine concentrations. Furthermore, the mRNA s of natriuretic peptides, neutrophil gelatinase‐associated lipocalin, hREN , and rR en were increased by vitamin D depletion. Regulatory T cells in the spleen and in the circulation were not affected. Ang metabolites, including Ang II and the counter‐regulatory breakdown product Ang 1 to 7, were significantly up‐regulated in the vitamin D‐depleted groups, while ACE ‐1 and ACE ‐2 activities were not affected. Conclusions Short‐term severe vitamin D depletion aggravated hypertension and target‐organ damage in dTGR . Our data suggest that even short‐term severe vitamin D deficiency may directly promote hypertension and impacts on renin‐angiotensin system components that could contribute to target‐organ damage. The findings add to the evidence that vitamin D deficiency could also affect human hypertension.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.114.001417
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 2653953-6
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