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  1. Article ; Online: Recent Advances in Hypertension: Epigenetic Mechanism Involved in Development of Salt-Sensitive Hypertension.

    Fujita, Toshiro

    Hypertension (Dallas, Tex. : 1979)

    2022  Volume 80, Issue 4, Page(s) 711–718

    Abstract: This review highlights recent insights into the epigenetic mechanism of salt-sensitive hypertension from the fetus to the elderly population, mainly focusing on the DNA methylation and histone modification-mediated regulation of hypertension-associated ... ...

    Abstract This review highlights recent insights into the epigenetic mechanism of salt-sensitive hypertension from the fetus to the elderly population, mainly focusing on the DNA methylation and histone modification-mediated regulation of hypertension-associated genes. Maternal malnutrition during pregnancy induces upregulation of
    MeSH term(s) Aged ; Pregnancy ; Female ; Mice ; Humans ; Animals ; Hypertension/genetics ; Sodium Chloride/metabolism ; Sodium Chloride, Dietary/metabolism ; Kidney/metabolism ; Receptors, Mineralocorticoid/metabolism ; Epigenesis, Genetic
    Chemical Substances Sodium Chloride (451W47IQ8X) ; Sodium Chloride, Dietary ; Receptors, Mineralocorticoid
    Language English
    Publishing date 2022-12-30
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 423736-5
    ISSN 1524-4563 ; 0194-911X ; 0362-4323
    ISSN (online) 1524-4563
    ISSN 0194-911X ; 0362-4323
    DOI 10.1161/HYPERTENSIONAHA.122.20588
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1488: Show issues Location:
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  2. Book ; Conference proceedings: High-risk patients and multifactorial treatment

    Fujita, Toshiro

    ... based on a symposium held on April 28, 2006, in Lisbon, Portugal

    (The American journal of cardiology ; 100,3A = Suppl.)

    2007  

    Author's details guest ed.: Toshiro Fujita
    Series title The American journal of cardiology ; 100,3A = Suppl.
    Collection
    Language English
    Size 60J S. : Ill., graph. Darst.
    Publisher Elsevier
    Publishing place New York, NY
    Publishing country United States
    Document type Book ; Conference proceedings
    HBZ-ID HT015275417
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Ui IV Zs 73 -100,3A- verfügbar in Königswinter Königswinter

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  3. Book ; Conference proceedings: Olmesartan: a new A II antagonist in cardiovascular risk prevention

    Fujita, Toshiro

    a satellite symposium to the Eleventh European Meeting on Hypertension, 17 June 2001 [Milan, Italy]

    (Journal of human hypertension ; 16, Suppl. 2)

    2002  

    Event/congress European Meeting on Hypertension (11, 2001, Mailand)
    Author's details guest ed.: Toshiro Fujita
    Series title Journal of human hypertension ; 16, Suppl. 2
    Collection
    Language English
    Size S28 S. : Ill., graph. Darst.
    Publisher Nature Publ. Group
    Publishing place Basingstoke
    Publishing country Great Britain
    Document type Book ; Conference proceedings
    HBZ-ID HT013365974
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

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    Zs A 2380 -16,Suppl.2- not available for loan Zeitschriften-Lesesaal

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  4. Article ; Online: Synthesis of a diruthenium μ-η

    Takao, Toshiro / Shimogawa, Ryuichi / Fujita, Ryosuke / Egawa, Shu

    Dalton transactions (Cambridge, England : 2003)

    2023  Volume 52, Issue 45, Page(s) 16737–16753

    Abstract: The reaction of [ ... ...

    Abstract The reaction of [Cp
    Language English
    Publishing date 2023-11-21
    Publishing country England
    Document type Journal Article
    ZDB-ID 1472887-4
    ISSN 1477-9234 ; 1364-5447 ; 0300-9246 ; 1477-9226
    ISSN (online) 1477-9234 ; 1364-5447
    ISSN 0300-9246 ; 1477-9226
    DOI 10.1039/d3dt03187j
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Salt-Sensitive Hypertension and the Kidney.

    Nishimoto, Mitsuhiro / Griffin, Karen / Wynne, Brandi M / Fujita, Toshiro

    Hypertension (Dallas, Tex. : 1979)

    2024  

    Abstract: Salt-sensitive hypertension (SS-HT) is characterized by blood pressure elevation in response to high dietary salt intake and is considered to increase the risk of cardiovascular and renal morbidity. Although the mechanisms responsible for SS-HT are ... ...

    Abstract Salt-sensitive hypertension (SS-HT) is characterized by blood pressure elevation in response to high dietary salt intake and is considered to increase the risk of cardiovascular and renal morbidity. Although the mechanisms responsible for SS-HT are complex, the kidneys are known to play a central role in the development of SS-HT and the salt sensitivity of blood pressure (SSBP). Moreover, several factors influence renal function and SSBP, including the renin-angiotensin-aldosterone system, sympathetic nervous system, obesity, and aging. A phenotypic characteristic of SSBP is aberrant activation of the renin-angiotensin system and sympathetic nervous system in response to excessive salt intake. SSBP is also accompanied by a blunted increase in renal blood flow after salt loading, resulting in sodium retention and SS-HT. Obesity is associated with inappropriate activation of the aldosterone mineralocorticoid receptor pathway and renal sympathetic nervous system in response to excessive salt, and mineralocorticoid receptor antagonists and renal denervation attenuate sodium retention and inhibit salt-induced blood pressure elevation in obese dogs and humans. SSBP increases with age, which has been attributed to impaired renal sodium handling and a decline in renal function, even in the absence of kidney disease. Aging-associated changes in renal hemodynamics are accompanied by significant alterations in renal hormone levels and renal sodium handling, resulting in SS-HT. In this review, we focus mainly on the contribution of renal function to the development of SS-HT.
    Language English
    Publishing date 2024-03-28
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 423736-5
    ISSN 1524-4563 ; 0194-911X ; 0362-4323
    ISSN (online) 1524-4563
    ISSN 0194-911X ; 0362-4323
    DOI 10.1161/HYPERTENSIONAHA.123.21369
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1488: Show issues Location:
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  6. Article ; Online: Kidney and epigenetic mechanisms of salt-sensitive hypertension.

    Kawarazaki, Wakako / Fujita, Toshiro

    Nature reviews. Nephrology

    2021  Volume 17, Issue 5, Page(s) 350–363

    Abstract: Dietary salt intake increases blood pressure (BP) but the salt sensitivity of BP differs between individuals. The interplay of ageing, genetics and environmental factors, including malnutrition and stress, contributes to BP salt sensitivity. In adults, ... ...

    Abstract Dietary salt intake increases blood pressure (BP) but the salt sensitivity of BP differs between individuals. The interplay of ageing, genetics and environmental factors, including malnutrition and stress, contributes to BP salt sensitivity. In adults, obesity is often associated with salt-sensitive hypertension. The children of women who experience malnutrition during pregnancy are at increased risk of developing obesity, diabetes and salt-sensitive hypertension as adults. Similarly, the offspring of mice that are fed a low-protein diet during pregnancy develop salt-sensitive hypertension in association with aberrant DNA methylation of the gene encoding type 1A angiotensin II receptor (AT
    MeSH term(s) Aging/physiology ; Aldosterone/physiology ; Angiotensin II/physiology ; Animals ; DNA Methylation ; Fetal Nutrition Disorders/physiopathology ; Glucuronidase/physiology ; Humans ; Hypertension/etiology ; Klotho Proteins ; Obesity/complications ; Oxidative Stress ; Receptors, Mineralocorticoid/physiology ; Renal Circulation ; Sodium Chloride, Dietary/adverse effects ; Wnt Signaling Pathway/physiology
    Chemical Substances Receptors, Mineralocorticoid ; Sodium Chloride, Dietary ; Angiotensin II (11128-99-7) ; Aldosterone (4964P6T9RB) ; Glucuronidase (EC 3.2.1.31) ; Klotho Proteins (EC 3.2.1.31)
    Language English
    Publishing date 2021-02-24
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2490366-8
    ISSN 1759-507X ; 1759-5061
    ISSN (online) 1759-507X
    ISSN 1759-5061
    DOI 10.1038/s41581-021-00399-2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6334: Show issues Location:
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    Zs.MG 107: Show issues

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  7. Article ; Online: Role of Rho in Salt-Sensitive Hypertension.

    Kawarazaki, Wakako / Fujita, Toshiro

    International journal of molecular sciences

    2021  Volume 22, Issue 6

    Abstract: A high amount of salt in the diet increases blood pressure (BP) and leads to salt-sensitive hypertension in individuals with impaired renal sodium excretion. Small guanosine triphosphatase (GTP)ase Rho and Rac, activated by salt intake, play important ... ...

    Abstract A high amount of salt in the diet increases blood pressure (BP) and leads to salt-sensitive hypertension in individuals with impaired renal sodium excretion. Small guanosine triphosphatase (GTP)ase Rho and Rac, activated by salt intake, play important roles in the pathogenesis of salt-sensitive hypertension as key switches of intracellular signaling. Focusing on Rho, high salt intake in the central nervous system increases sodium concentrations of cerebrospinal fluid in salt-sensitive subjects via Rho/Rho kinase and renin-angiotensin system activation and causes increased brain salt sensitivity and sympathetic nerve outflow in BP control centers. In vascular smooth muscle cells, Rho-guanine nucleotide exchange factors and Rho determine sensitivity to vasoconstrictors such as angiotensin II (Ang II), and facilitate vasoconstriction via G-protein and Wnt pathways, leading to increased vascular resistance, including in the renal arteries, in salt-sensitive subjects with high salt intake. In the vascular endothelium, Rho/Rho kinase inhibits nitric oxide (NO) production and function, and high salt amounts further augment Rho activity via asymmetric dimethylarginine, an endogenous inhibitor of NO synthetase, causing aberrant relaxation and increased vascular tone. Rho-associated mechanisms are deeply involved in the development of salt-sensitive hypertension, and their further elucidation can help in developing effective protection and new therapies.
    MeSH term(s) Angiotensin II/genetics ; Blood Pressure/drug effects ; Humans ; Hypertension/chemically induced ; Hypertension/genetics ; Hypertension/pathology ; Nitric Oxide/genetics ; Nitric Oxide Synthase/genetics ; Sodium Chloride, Dietary/adverse effects ; Sympathetic Nervous System/drug effects ; Sympathetic Nervous System/metabolism ; Vasoconstriction/genetics ; rho-Associated Kinases/genetics
    Chemical Substances Sodium Chloride, Dietary ; Angiotensin II (11128-99-7) ; Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase (EC 1.14.13.39) ; rho-Associated Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2021-03-15
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms22062958
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  8. Article ; Online: The Mineralocorticoid Receptor in Salt-Sensitive Hypertension and Renal Injury.

    Ayuzawa, Nobuhiro / Fujita, Toshiro

    Journal of the American Society of Nephrology : JASN

    2021  Volume 32, Issue 2, Page(s) 279–289

    Abstract: Hypertension and its comorbidities pose a major public health problem associated with disease-associated factors related to a modern lifestyle, such high salt intake or obesity. Accumulating evidence has demonstrated that aldosterone and its receptor, ... ...

    Abstract Hypertension and its comorbidities pose a major public health problem associated with disease-associated factors related to a modern lifestyle, such high salt intake or obesity. Accumulating evidence has demonstrated that aldosterone and its receptor, the mineralocorticoid receptor (MR), have crucial roles in the development of salt-sensitive hypertension and coexisting cardiovascular and renal injuries. Accordingly, clinical trials have repetitively shown the promising effects of MR blockers in these diseases. We and other researchers have identified novel mechanisms of MR activation involved in salt-sensitive hypertension and renal injury, including the obesity-derived overproduction of aldosterone and ligand-independent signaling. Moreover, recent advances in the analysis of cell-specific and context-dependent mechanisms of MR activation in various tissues-including a classic target of aldosterone, aldosterone-sensitive distal nephrons-are now providing new insights. In this review, we summarize recent updates to our understanding of aldosterone-MR signaling, focusing on its role in salt-sensitive hypertension and renal injury.
    MeSH term(s) Acute Kidney Injury/etiology ; Aldosterone/physiology ; Humans ; Hypertension/etiology ; Metabolic Syndrome/etiology ; Receptors, Mineralocorticoid/physiology ; Renin-Angiotensin System/physiology ; Sodium Chloride, Dietary
    Chemical Substances Receptors, Mineralocorticoid ; Sodium Chloride, Dietary ; Aldosterone (4964P6T9RB)
    Language English
    Publishing date 2021-01-04
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1085942-1
    ISSN 1533-3450 ; 1046-6673
    ISSN (online) 1533-3450
    ISSN 1046-6673
    DOI 10.1681/ASN.2020071041
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 3344: Show issues Location:
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  9. Article ; Online: Role of Rho in Salt-Sensitive Hypertension

    Wakako Kawarazaki / Toshiro Fujita

    International Journal of Molecular Sciences, Vol 22, Iss 2958, p

    2021  Volume 2958

    Abstract: A high amount of salt in the diet increases blood pressure (BP) and leads to salt-sensitive hypertension in individuals with impaired renal sodium excretion. Small guanosine triphosphatase (GTP)ase Rho and Rac, activated by salt intake, play important ... ...

    Abstract A high amount of salt in the diet increases blood pressure (BP) and leads to salt-sensitive hypertension in individuals with impaired renal sodium excretion. Small guanosine triphosphatase (GTP)ase Rho and Rac, activated by salt intake, play important roles in the pathogenesis of salt-sensitive hypertension as key switches of intracellular signaling. Focusing on Rho, high salt intake in the central nervous system increases sodium concentrations of cerebrospinal fluid in salt-sensitive subjects via Rho/Rho kinase and renin-angiotensin system activation and causes increased brain salt sensitivity and sympathetic nerve outflow in BP control centers. In vascular smooth muscle cells, Rho-guanine nucleotide exchange factors and Rho determine sensitivity to vasoconstrictors such as angiotensin II (Ang II), and facilitate vasoconstriction via G-protein and Wnt pathways, leading to increased vascular resistance, including in the renal arteries, in salt-sensitive subjects with high salt intake. In the vascular endothelium, Rho/Rho kinase inhibits nitric oxide (NO) production and function, and high salt amounts further augment Rho activity via asymmetric dimethylarginine, an endogenous inhibitor of NO synthetase, causing aberrant relaxation and increased vascular tone. Rho-associated mechanisms are deeply involved in the development of salt-sensitive hypertension, and their further elucidation can help in developing effective protection and new therapies.
    Keywords Rho ; Rac ; salt-sensitive hypertension ; salt ; blood pressure ; angiotensin II ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 571
    Language English
    Publishing date 2021-03-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  10. Article ; Online: Novel mechanisms of salt-sensitive hypertension.

    Vogt, Liffert / Marques, Francine Z / Fujita, Toshiro / Hoorn, Ewout J / Danser, A H Jan

    Kidney international

    2023  Volume 104, Issue 4, Page(s) 690–697

    Abstract: A high dietary sodium-consumption level is considered the most important lifestyle factor that can be modified to help prevent an increase in blood pressure and the development of hypertension. Despite numerous studies over the past decades, the ... ...

    Abstract A high dietary sodium-consumption level is considered the most important lifestyle factor that can be modified to help prevent an increase in blood pressure and the development of hypertension. Despite numerous studies over the past decades, the pathophysiology explaining why some people show a salt-sensitive blood pressure response and others do not is incompletely understood. Here, a brief overview of the latest mechanistic insights is provided, focusing on the mononuclear phagocytic system and inflammation, the gut-kidney axis, and epigenetics. The article also discusses the effects of 3 types of novel drugs on salt-sensitive hypertension-sodium-glucose cotransporter 2 inhibitors, nonsteroidal mineralocorticoid receptor antagonists, and aldosterone synthase inhibitors. The conclusion is that besides kidney-centered mechanisms, vasoconstrictor mechanisms are also relevant for both the understanding and treatment of this blood pressure phenotype.
    MeSH term(s) Humans ; Aldosterone ; Blood Pressure ; Hypertension/genetics ; Mineralocorticoid Receptor Antagonists/pharmacology ; Receptors, Mineralocorticoid ; Sodium Chloride, Dietary/adverse effects
    Chemical Substances Aldosterone (4964P6T9RB) ; Mineralocorticoid Receptor Antagonists ; Receptors, Mineralocorticoid ; Sodium Chloride, Dietary
    Language English
    Publishing date 2023-07-14
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2023.06.035
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