Molecular Mechanisms of Human Hypertension

By R. Lifton, Ali G. Gharavi, David S. Geller. Cell, 2001

1,703 citations recorded by the source corpus.

Subfields: Endocrinology, Diabetes and Metabolism, Molecular Biology, Pharmacology

View Paper: https://www.semanticscholar.org/paper/f9039a3dffd95325deaa8927769a522f35be31bf

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Endocrinology, Diabetes and Metabolism

1. G. MacGregor
2. F. He

In Molecular Biology

1. G. MacGregor
2. F. He
3. Shrikant M. Mane

In Pharmacology

1. G. MacGregor
2. F. He

Citations in the corpus

• G12-G13–LARG–mediated signaling in vascular smooth muscle is required for salt-induced hypertension (2008, neutral): “Most forms of hypertension ultimately result from an increased vascular tone that leads to an elevated total peripheral resistanc”
• Links between dietary salt intake, renal salt handling, blood pressure, and cardiovascular diseases. (2005, positive): “With the use of association or linkage studies and positional cloning during the last decade, over 20 genes associated with essential hypertension or responsible for rare Mendelian diseases with high or low blood pressure have been identified in humans to date (213).”
• Rare independent mutations in renal salt handling genes contribute to blood pressure variation (2008, neutral): “The study of rare mendelian traits has identified more than 20 genes in which mutations impart large effects on blood pressure; these predominantly act by changing net renal salt reabsorptio”
• ESH / ESC Guidelines for the management of arterial hypertension (2013, neutral): “tation fully explains the pathogenesis of hypertension and dictates the best treatment modality.(147) Essential hypertension is a highly heterogeneous disorder with amultifactorial aetiology.”
• 2013 ESH/ESC Guidelines for the management of arterial hypertension (2007, neutral): “Several rare, monogenic forms of hypertension have been described, such as glucocorticoid-remediable aldosteronism, Liddle’s syndrome and others, where a single gene mutation fully explains the pathogenesis of hypertension and dictates the best treatment modality [147].”
• Reducing population salt intake worldwide: from evidence to implementation. (2010, positive): “Molecular genetic studies in humans have identified mutations in several genes that cause Mendelian forms of hypertension or hypotension.(20) All of these affect the kidney's ability to excrete sodium, and salt intake has dramatic effects on BP in these individuals.”
• Macrophages regulate salt-dependent volume and blood pressure by a vascular endothelial growth factor-C–dependent buffering mechanism (2009, neutral): “This hypothesis is supported by the fact that monogenic forms of hypertension involves renal channels and transporters that predispose the body to extracellular sodium retentio”
• Discovering genotypes underlying human phenotypes: past successes for mendelian disease, future approaches for complex disease (2003, neutral): “An outstanding example of the success of the 'well-informed candidate gene' approach has been the systematic cloning of genes in which mutations cause severely high or low blood pressur”
• The 2015 Canadian Hypertension Education Program recommendations for blood pressure measurement, diagnosis, assessment of risk, prevention, and treatment of hypertension. (2013, neutral): “Several rare, monogenic forms of hypertension have been described, such as glucocorticoid-remediable aldosteronism, Liddle’s syndrome and others, where a single gene mutation fully explains the pathogenesis of hypertension and dictates the best treatment modality [147].”