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  1. Article ; Online: Correction to: Histamine H2‑receptor antagonism improves conduit artery endothelial function and reduces plasma aldosterone level without lowering arterial blood pressure in angiotensin II-hypertensive mice.

    Assersen, Kasper B / Jensen, Boye L / Enggaard, Camilla / Vanhoutte, Paul M / Hansen, Pernille B L

    Pflugers Archiv : European journal of physiology

    2024  Volume 476, Issue 5, Page(s) 871

    Language English
    Publishing date 2024-03-27
    Publishing country Germany
    Document type Published Erratum
    ZDB-ID 6380-0
    ISSN 1432-2013 ; 0031-6768
    ISSN (online) 1432-2013
    ISSN 0031-6768
    DOI 10.1007/s00424-024-02955-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Histamine H

    Assersen, Kasper B / Jensen, Boye L / Enggaard, Camilla / Vanhoutte, Paul M / Hansen, Pernille B L

    Pflugers Archiv : European journal of physiology

    2024  Volume 476, Issue 3, Page(s) 307–321

    Abstract: Aldosterone through the mineralocorticoid receptor MR has detrimental effects on cardiovascular disease. It reduces the bioavailability of nitric oxide and impairs endothelium-dependent vasodilatation. In resistance arteries, aldosterone impairs the ... ...

    Abstract Aldosterone through the mineralocorticoid receptor MR has detrimental effects on cardiovascular disease. It reduces the bioavailability of nitric oxide and impairs endothelium-dependent vasodilatation. In resistance arteries, aldosterone impairs the sensitivity of vascular smooth muscle cells to nitric oxide by promoting the local secretion of histamine which activates H
    MeSH term(s) Mice ; Animals ; Aldosterone ; Angiotensin II/pharmacology ; Arterial Pressure ; Histamine/pharmacology ; Histamine H2 Antagonists/adverse effects ; Ranitidine/adverse effects ; Nitric Oxide ; Hypertension ; Blood Pressure ; Endothelium, Vascular ; Mesenteric Arteries
    Chemical Substances Aldosterone (4964P6T9RB) ; Angiotensin II (11128-99-7) ; Histamine (820484N8I3) ; Histamine H2 Antagonists ; Ranitidine (884KT10YB7) ; Nitric Oxide (31C4KY9ESH)
    Language English
    Publishing date 2024-01-27
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 6380-0
    ISSN 1432-2013 ; 0031-6768
    ISSN (online) 1432-2013
    ISSN 0031-6768
    DOI 10.1007/s00424-024-02909-0
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  3. Article ; Online: The Renin-Angiotensin System in Hypertension, a Constantly Renewing Classic: Focus on the Angiotensin AT

    Assersen, Kasper B / Sumners, Colin / Steckelings, U Muscha

    The Canadian journal of cardiology

    2020  Volume 36, Issue 5, Page(s) 683–693

    Abstract: It is common knowledge that the renin-angiotensin system (RAS), in particular angiotensin II acting through the angiotensin ... ...

    Abstract It is common knowledge that the renin-angiotensin system (RAS), in particular angiotensin II acting through the angiotensin AT
    MeSH term(s) Brain/physiology ; Endothelium, Vascular/metabolism ; Female ; Humans ; Hypertension/physiopathology ; Nitric Oxide/metabolism ; Nitric Oxide Synthase/metabolism ; Pre-Eclampsia/physiopathology ; Pregnancy ; Receptor, Angiotensin, Type 2/physiology ; Renin-Angiotensin System/physiology ; Vasodilation/physiology
    Chemical Substances Receptor, Angiotensin, Type 2 ; Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase (EC 1.14.13.39)
    Language English
    Publishing date 2020-03-05
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 632813-1
    ISSN 1916-7075 ; 0828-282X
    ISSN (online) 1916-7075
    ISSN 0828-282X
    DOI 10.1016/j.cjca.2020.02.095
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  4. Article ; Online: Natriuretic peptides relax human intrarenal arteries through natriuretic peptide receptor type-A recapitulated by soluble guanylyl cyclase agonists.

    Frees, Andreas / Assersen, Kasper B / Jensen, Mia / Hansen, Pernille B L / Vanhoutte, Paul M / Madsen, Kirsten / Federlein, Anna / Lund, Lars / Toft, Anja / Jensen, Boye L

    Acta physiologica (Oxford, England)

    2020  Volume 231, Issue 3, Page(s) e13565

    Abstract: Aim: Natriuretic peptides, BNP and ANP increase renal blood flow in experimental animals. The signalling pathway in human kidney vasculature is unknown. It was hypothesized that BNP and ANP cause endothelium-independent relaxation of human intrarenal ... ...

    Abstract Aim: Natriuretic peptides, BNP and ANP increase renal blood flow in experimental animals. The signalling pathway in human kidney vasculature is unknown. It was hypothesized that BNP and ANP cause endothelium-independent relaxation of human intrarenal arteries by vascular natriuretic peptide receptor-A, but not -B and -C, which is mimicked by agonists of soluble guanylyl cyclase sGC.
    Methods: Human (n = 54, diameter: 665 ± 29 µm 95% CI) and control murine intrarenal arteries (n = 83, diameter 300 ± 6 µm 95% CI) were dissected and used for force recording by four-channel wire myography. Arterial segments were pre-contracted, then subjected to increasing concentrations of BNP, ANP, phosphodiesterase 5-inhibitor sildenafil, sGC-activator BAY 60-2770 and -stimulator BAY 41-2272. Endothelial nitric oxide synthase (eNOS) dependence was examined by use of L-NAME and eNOS knockout respectively. Molecular targets (NPR A-C, sGC, phosphodiesterase-5 and neprilysin) were mapped by PCR, immunohistochemistry and RNAscope.
    Results: BNP, ANP, sildenafil, sGC-activation and -stimulation caused concentration-dependent relaxation of human and murine intrarenal arteries. BNP responses were independent of eNOS and were not potentiated by low concentration of phosphodiesterase-5-inhibitor, sGC-stimulator or NPR-C blocker. PCR showed NPR-A and C, phosphodiesterase-5, neprilysin and sGC mRNA in renal arteries. NPR-A mRNA and protein was observed in vascular smooth muscle and endothelial cells in arteries, podocytes, Bowmans capsule and vasa recta. NPR-C was observed in tubules, glomeruli and vasculature.
    Conclusion: Activation of transmembrane NPR-A and soluble guanylyl cyclase relax human preglomerular arteries similarly to phosphodiestase-5 inhibition. The human renal arterial bed relaxes in response to cGMP pathway.
    MeSH term(s) Animals ; Arteries ; Cyclic GMP ; Endothelial Cells ; Guanylate Cyclase ; Humans ; Mice ; Natriuretic Peptides/pharmacology ; Soluble Guanylyl Cyclase
    Chemical Substances Natriuretic Peptides ; Guanylate Cyclase (EC 4.6.1.2) ; Soluble Guanylyl Cyclase (EC 4.6.1.2) ; Cyclic GMP (H2D2X058MU)
    Language English
    Publishing date 2020-11-05
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2218636-0
    ISSN 1748-1716 ; 1748-1708
    ISSN (online) 1748-1716
    ISSN 1748-1708
    DOI 10.1111/apha.13565
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  5. Article ; Online: The exaggerated natriuresis of essential hypertension occurs independently of changes in renal medullary blood flow.

    Assersen, Kasper B / Høilund-Carlsen, Poul F / Olsen, Michael H / Greve, Sara V / Gam-Hadberg, Jens C / Braad, Poul-Erik / Damkjaer, Mads / Bie, Peter

    Acta physiologica (Oxford, England)

    2019  Volume 226, Issue 3, Page(s) e13266

    Abstract: Aims: In patients with essential hypertension, abnormal renal sodium handling includes exaggerated natriuresis in response to extracellular volume expansion. We tested the hypothesis that exaggerated natriuresis is associated with increases in medullary ...

    Abstract Aims: In patients with essential hypertension, abnormal renal sodium handling includes exaggerated natriuresis in response to extracellular volume expansion. We tested the hypothesis that exaggerated natriuresis is associated with increases in medullary and/or cortical renal blood flow.
    Methods: Patients with mild essential hypertension, but no signs of end organ damage, and control subjects were studied after 4 days of dietary standardization (<60 mmol Na
    Results: In patients, arterial blood pressure increased during volume expansion (107 ± 2-114 ± 3 mm Hg, P < 0.05) in contrast to the control group (92 ± 2-92 ± 2 mm Hg). Renal sodium excretion increased more in patients than in controls (+133 ± 31 µmol min
    Conclusion: Exaggerated natriuresis, a hallmark of essential hypertension, is not mediated by increases in regional, renal blood flow.
    MeSH term(s) Adult ; Blood Pressure/physiology ; Essential Hypertension/physiopathology ; Female ; Glomerular Filtration Rate/physiology ; Hemodynamics/physiology ; Humans ; Hypertension/physiopathology ; Kidney Medulla/physiology ; Male ; Middle Aged ; Natriuresis/physiology ; Regional Blood Flow/physiology ; Renal Circulation/physiology
    Language English
    Publishing date 2019-03-12
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2218636-0
    ISSN 1748-1716 ; 1748-1708
    ISSN (online) 1748-1716
    ISSN 1748-1708
    DOI 10.1111/apha.13266
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  6. Article ; Online: Periarterial fat from two human vascular beds is not a source of aldosterone to promote vasoconstriction.

    Assersen, Kasper B / Jensen, Pia S / Briones, Ana M / Rasmussen, Lars M / Marcussen, Niels / Toft, Anja / Vanhoutte, Paul M / Jensen, Boye L / Hansen, Pernille B L

    American journal of physiology. Renal physiology

    2018  Volume 315, Issue 6, Page(s) F1670–F1682

    Abstract: Mouse adipocytes have been reported to release aldosterone and reduce endothelium-dependent relaxation. It is unknown whether perivascular adipose tissue (PVAT) releases aldosterone in humans. The present experiments were designed to test the hypothesis ... ...

    Abstract Mouse adipocytes have been reported to release aldosterone and reduce endothelium-dependent relaxation. It is unknown whether perivascular adipose tissue (PVAT) releases aldosterone in humans. The present experiments were designed to test the hypothesis that human PVAT releases aldosterone and induces endothelial dysfunction. Vascular reactivity was assessed in human internal mammary and renal segmental arteries obtained at surgery. The arteries were prepared with/without PVAT, and changes in isometric tension were measured in response to the vasoconstrictor thromboxane prostanoid receptor agonist U46619 and the endothelium-dependent vasodilator acetylcholine. The effects of exogenous aldosterone and of mineralocorticoid receptor (MR) antagonist eplerenone were determined. Aldosterone concentrations were measured by ELISA in conditioned media incubated with human adipose tissue with/without angiotensin II stimulation. Presence of aldosterone synthase and MR mRNA was examined in perirenal, abdominal, and mammary PVAT by PCR. U46619 -induced tension and acetylcholine-induced relaxation were unaffected by exogenous and endogenous aldosterone (addition of aldosterone and MR blocker) in mammary and renal segmental arteries, both in the presence and absence of PVAT. Aldosterone release from incubated perivascular fat was not detectable. Aldosterone synthase expression was not consistently observed in human adipose tissues in contrast to that of MR. Thus, exogenous aldosterone does not affect vascular reactivity and endothelial function in ex vivo human arterial segments, and the tested human adipose tissues have no capacity to synthesize/release aldosterone. In perspective, physiologically relevant effects of aldosterone on vascular function in humans are caused by systemic aldosterone originating from the adrenal gland.
    MeSH term(s) Adipose Tissue/metabolism ; Aged ; Aldosterone/metabolism ; Culture Media, Conditioned/metabolism ; Female ; Humans ; Male ; Mammary Arteries/metabolism ; Mammary Arteries/surgery ; Middle Aged ; Paracrine Communication ; Renal Artery/metabolism ; Renal Artery/surgery ; Secretory Pathway ; Signal Transduction ; Tissue Culture Techniques ; Vasoconstriction
    Chemical Substances Culture Media, Conditioned ; Aldosterone (4964P6T9RB)
    Language English
    Publishing date 2018-10-03
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00391.2018
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