Genomic Expression Systems on Hierarchy and Network Leading to Hypertension: Long on History, Short on Facts.

Fukamizu, Akiyoshi

doi:10.1291/hypres.23.545

Cited by 5 publications

(4 citation statements)

References 65 publications

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“…However, more data on the regulation of distal tubular renin expression, especially in hypertensive conditions, are needed [74]. This functional analysis is consistent with and provides further support to the genetic studies suggesting a linkage between variations in the AGT gene and hypertension [75,85]. .…”

Section: Discussionsupporting

confidence: 76%

Intrarenal angiotensin II and hypertension

Navar

Kobori²,

Prieto-Carrasquero³

2003

Current Science Inc

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Elevations in intrarenal angiotensin II (Ang II) cause reductions in renal function and sodium excretion that contribute to progressive hypertension and lead to renal and vascular injury. Augmentation of intrarenal Ang II occurs by several processes, leading to levels much greater than can be explained from the circulating levels. In Ang II-dependent hypertension, Ang II is internalized via an AT1 receptor mechanism, but there is also sustained intrarenal production of Ang II. Ang II exerts a positive feedback action on intrarenal angiotensinogen (AGT) mRNA and protein. The increased intrarenal AGT production is associated with increased intrarenal and intracellular Ang II contents and urinary AGT excretion rates. The increased urinary AGT indicates spillover of AGT into distal nephron segments supporting enhanced distal Ang II formation and sodium reabsorption. The augmentation of intrarenal Ang II provides the basis for sustained actions on renal function, sodium excretion, and maintenance of hypertension.

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Section: Discussionsupporting

confidence: 76%

Intrarenal angiotensin II and hypertension

Navar

Kobori²,

Prieto-Carrasquero³

2003

Current Science Inc

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“…However, these experiments were not designed carefully enough and are thus without further meaning for future gene therapy (see below). With regard to hywell-known blood pressure regulating systems; however, the meaning of these animal models for the development of a therapy against the human disease was only speculative in terms like "might be a promising model for the future" or "requires further research" or similar phrases (Audoloy et al, 2000;Bader et al, 2000;lake-Bruse and Sigmund, 2000;Fukamizu, 2000;Cvetkovic and Sigmund, 2000;Yagil and Yagil, 2001;Sugiyama et al, 2001;lavoie et al, 2004;Barbosa et al, 2005;lerman et al, 2005;McBride et al, 2006). the remaining 8 reviews (42%) were more critical and emphasised the limitations of the animal models when used to try to understand and treat human hypertension (Kurihara, 2001;Mullins and Mullins, 2003;takahashi and Smithies, 2004;Herrera and Ruiz-Opazo, 2005;Smithies, 2005;Bernstein et al, 2005;.…”

Section: B) General Overview Of Animal Models For Human Hypertensionmentioning

confidence: 99%

20 Years of Hypertension Research using Genetically Modified Animals: No Clinically Promising Approaches in Sight

Stingl

Völkel²,

Lindl³

2009

ALTEX

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“…Several rat models of genetic hypertension have been developed to study the genetic determinants of blood pressure (BP) regulation (1)(2)(3). The inbred Dahl salt-sensitive (SS/Jr or S) rat is the most widely studied genetic model of salt-sensitive hypertension (4).…”

Section: Introductionmentioning

confidence: 99%

Use of a Panel of Congenic Strains to Evaluate Differentially Expressed Genes as Candidate Genes for Blood Pressure Quantitative Trait Loci.

Cha

Liu

et al. 2003

Hypertens Res

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otherwise similar genetic composition derived from S rats, constitute a powerful and unique tool for identifying strong candidate genes for BP QTL (1).The toughest impediment to understanding the molecular basis of hypertension is proceeding from chromosomal locations associated with BP QTL to determining what genes in those chromosomal regions are causative for the observed differences in BP. A methodology must be developed to rapidly identify and characterize strong candidate genes for QTLs. The development of congenic strains and substrains has become a key method for limiting the chromosomal region that contains gene(s) responsible for the effect of a given QTL. Many congenic strains have already been developed to study the genetic basis of quantitative traits of both clinical and commercial importance, including BP. As described above, a panel of such congenic strains could be used to help

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Genomic Expression Systems on Hierarchy and Network Leading to Hypertension: Long on History, Short on Facts.

Cited by 5 publications

References 65 publications

Intrarenal angiotensin II and hypertension

Intrarenal angiotensin II and hypertension

20 Years of Hypertension Research using Genetically Modified Animals: No Clinically Promising Approaches in Sight

Use of a Panel of Congenic Strains to Evaluate Differentially Expressed Genes as Candidate Genes for Blood Pressure Quantitative Trait Loci.

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