ArticleHypertension (Dallas, Tex. : 1979)2015
Critical Role of Striatin in Blood Pressure and Vascular Responses to Dietary Sodium Intake.
Article in Hypertension (Dallas, Tex. : 1979), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03683069 (Hypertension and Striatin Gene Structure Related to Aldo Phenotype), which is not on this map. Cited by 16 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Hypertension and Striatin Gene Structure Related to Aldo Phenotype
Who cites it
16 citing papers in PubMed, 31 citations in OpenAlex.
- Targeting PP2A in cancer: an underrated option.Journal of experimental & clinical cancer research : CR · 2025Review
- The foam cell-derived exosomal miRNA Novel-3 drives neuroinflammation and ferroptosis during ischemic stroke.Nature aging · 2024Article
- Striatin plays a major role in angiotensin II-induced cardiomyocyte and cardiac hypertrophy in mice in vivo.Clinical science (London, England : 1979) · 2024Article
- Placental expression of striatin & endothelial nitric oxide synthase in women with & without pre-eclampsia.The Indian journal of medical research · 2023Article
- The Effect of Aldosterone on Cardiorenal and Metabolic Systems.International journal of molecular sciences · 2023Review
- Enhanced Thrombotic Responses Are Associated With Striatin Deficiency and Aldosterone.Journal of the American Heart Association · 2021Article
- The Interface of Nuclear and Membrane Steroid Signaling.Endocrinology · 2021Review
- The STRIPAK signaling complex regulates dephosphorylation of GUL1, an RNA-binding protein that shuttles on endosomes.PLoS genetics · 2020Article
- Striatin heterozygous mice are more sensitive to aldosterone-induced injury.The Journal of endocrinology · 2020Article
- High STRN Expression Promotes HCC Invasion and Migration but Not Cell Proliferation or Apoptosis through Facilitating Epithelial-Mesenchymal Transition.BioMed research international · 2020Article
- Aldosterone Rapidly Enhances Levels of the Striatin and Caveolin-1 Proteins in Rat Kidney: The Role of the Mineralocorticoid Receptor.Endocrinology and metabolism (Seoul, Korea) · 2019Article
- Precise and systematic survey of the efficacy of multicomponent drugs against functional dyspepsia.Scientific reports · 2019Article
- Genetics of Human Primary Hypertension: Focus on Hormonal Mechanisms.Endocrine reviews · 2019Review
- Article
- 17β-estradiol upregulates striatin protein levels via Akt pathway in human umbilical vein endothelial cells.PloS one · 2018Article
- Striatin Gene Polymorphic Variants Are Associated With Salt Sensitive Blood Pressure in Normotensives and Hypertensives.American journal of hypertension · 2017Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Striatin is a protein regulator of vesicular trafficking in neurons that also binds caveolin-1 and Ca(2+)-calmodulin and could activate endothelial nitric oxide synthase. We have shown that striatin colocalizes with the mineralocorticoid receptor and that mineralocorticoid receptor activation increases striatin levels in vascular cells. To test whether striatin is a regulator of vascular function, wild-type and heterozygous striatin-deficient mice (Strn(+/-)) were randomized in crossover intervention to restricted (0.03%) and liberal sodium (1.6%) diets for 7 days on each diet, and blood pressure and aortic vascular function were measured. Compared with wild-type, sodium restriction significantly reduced blood pressure in Strn(+/-). On liberal salt intake, phenylephrine and high KCl caused a greater vascular contraction in Strn(+/-) than wild-type, and endothelium removal, nitric oxide synthase inhibitor L-NAME, and guanylate cyclase inhibitor ODQ enhanced phenylephrine contraction to a smaller extent in Strn(+/-) than wild-type. On liberal salt, acetylcholine relaxation was less in Strn(+/-) than in wild-type, and endothelium removal, L-NAME, and ODQ blocked acetylcholine relaxation, suggesting changes in endothelial NO-cGMP. On liberal salt, endothelial nitric oxide synthase mRNA expression and the ratio of endothelial nitric oxide synthase activator pAkt/total Akt were decreased in Strn(+/-) versus wild-type. Vascular relaxation to NO donor sodium nitroprusside was not different among groups. Thus, striatin deficiency is associated with salt sensitivity of blood pressure, enhanced vasoconstriction, and decreased vascular relaxation, suggesting a critical role for striatin, through modulation of endothelial NO-cGMP, in regulation of vascular function and BP during changes in sodium intake.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.