Browsing by Author "Williams, Gordon H."

Now showing 1 - 5 of 5
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    A prevalent caveolin-1 gene variant is associated with the metabolic syndrome in Caucasians and Hispanics
    (2015) Baudrand Biggs, René; Goodarzi, Mark O.; Vaidya, Anand; Underwood, Patricia C.; Williams, Jonathan S.; Jeunemaitre, Xavier; Hopkins, Paul N.; Brown, Nancy; Raby, Benjamin A.; Lasky-Su, Jessica; Adler, Gail K.; Cui, Jinrui; Guo, Xiuqing; Taylor, Kent D.; Chen, Yii-Der I.; Xiang, Anny; Raffel, Leslie J.; Buchanan, Thomas A.; Rotter, Jerome I.; Williams, Gordon H.; Pojoga, Luminita H.
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    Renin Phenotypes Characterize Vascular Disease, Autonomous Aldosteronism, and Mineralocorticoid Receptor Activity
    (2017) Hundemer, Gregory L.; Baudrand Biggs, René; Brown, Jenifer M.; Curhan, Gary; Williams, Gordon H.; Vaidya, Anand
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    Statin Use and Adrenal Aldosterone Production in Hypertensive and Diabetic Subjects
    (2015) Baudrand Biggs, René; Pojoga, Luminita H.; Vaidya, Anand; Garza, Amanda; Vohringer, Paul A.; Jeunemaitre, Xavier; Hopkins, Paul N.; Yao, Tham M.; Williams, Jonathan; Adler, Gail K.; Williams, Gordon H.
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    Striatin heterozygous mice are more sensitive to aldosterone-induced injury
    (2020) Garza, Amanda E.; Trefts, Elijah; Rangel, Isis A. Katayama; Brooks, Danielle; Baudrand, Rene; Moize, Burhanuddin; Romero, Jose R.; Ranjit, Sanjay; Treesaranuwattana, Thitinan; Yao, Tham M.; Adler, Gail K.; Pojoga, Luminita H.; Williams, Gordon H.
    Aldosterone modulates the activity of both epithelial (specifically renal) and non-epithelial cells. Binding to the mineralocorticoid receptor (MR), activates two pathways: the classical genomic and the rapidly activated non-genomic that is substantially modulated by the level of striatin. We hypothesized that disruption of MR's non-genomic pathway would alter aldosterone-induced cardiovascular/renal damage. To test this hypothesis, wild type (WT) and striatin heterozygous knockout (Strn(+/-)) littermate male mice were fed a liberal sodium (1.6% Na+) diet and randomized to either protocol one: 3 weeks of treatment with either vehicle or aldosterone plus/minus MR antagonists, eplerenone or esaxerenone or protocol two: 2 weeks of treatment with either vehicle or L-NAME/Angll plus/minus MR antagonists, spironolactone or esaxerenone. Compared to the WT mice, basally, the Strn(+/-) mice had greater (similar to 26%) estimated renal glomeruli volume and reduced non-genomic second messenger signaling (pAkt/Akt ratio) in kidney tissue. In response to active treatment, the striatin-associated-cardiovascular/renal damage was limited to volume effects induced by aldosterone infusion: significantly increased blood pressure (BP) and albuminuria. In contrast, with aldosterone or L-NAME/Angll treatment, striatin deficiency did not modify aldosterone-mediated damage: in the heart and kidney, macrophage infiltration, and increases in aldosterone-induced biomarkers of injury. All changes were near-normalized following MR blockade with spironolactone or esaxerenone, except increased BP in the L-NAME/Angll model. In conclusion, the loss of striatin amplified aldosterone-induced damage suggesting that aldosterone's non-genomic pathway is protective but only related to effects likely mediated via epithelial, but not non-epithelial cells.
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    Variants in Striatin Gene Are Associated With Salt-Sensitive Blood Pressure in Mice and Humans
    (2015) Garza, Amanda E.; Rariy, Chevon M.; Sun, Bei; Williams, Jonathan S.; Lasky-Su, Jessica; Baudrand Biggs, René; Yao, Tham; Moize, Burhanuddin; Hafiz, Wan M.; Romero, José R.; Adler, Gail K.; Ferri, Claudio; Hopkins, Paul N.; Pojoga, Luminita H.; Williams, Gordon H.