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Gordon H. Williams

Researcher at Brigham and Women's Hospital

Publications -  563
Citations -  39948

Gordon H. Williams is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: Angiotensin II & Aldosterone. The author has an hindex of 88, co-authored 559 publications receiving 38048 citations. Previous affiliations of Gordon H. Williams include University of Sydney & University of Michigan.

Papers
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Aldosterone's mechanism of action: roles of lysine-specific demethylase 1, caveolin and striatin.

TL;DR: New mediators of aldosterone's mechanisms of action are described: lysine-specific demethylase 1 (LSD1), caveolin 1 (cav-1) and striatin, a scaffolding protein that mediates a novel interaction between signalling molecules and mineralocorticoid receptor's rapid effects in the cardiovascular system.
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Erratum: New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk (Nature Genetics (2010) 42 (105-116))

Josée Dupuis, +303 more
- 01 May 2010 - 
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Renin gene polymorphism: its relationship to hypertension, renin levels and vascular responses

TL;DR: Results confirm that polymorphisms in the renin gene are associated with increased risk for hypertension in an independent cohort, and that the underlying mechanism may reside in the interaction of renin activity and vascular responsiveness to angiotensin II.
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Renin suppression by saline is blunted in nonmodulating essential hypertension.

TL;DR: Nonmodulating essential hypertensive patients have abnormalities in several systems that influence sodium homeostasis, including altered adrenal and renal vascular response to angiotensin II, altered renal blood flow response to salt loading, and a delayed suppression of the renin-angiotens in-aldosterone system with short-term saline infusion.
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Effects of gender and genotype on the phenotypic expression of nonmodulating essential hypertension.

TL;DR: The genetic and gender data recently available suggest that the expression of the nonmodulating phenotype, presumably secondary to changes in theexpression of the angiotensinogen gene, is modulated by female sex hormones.