Journal
CURRENT HYPERTENSION REVIEWS
Volume 10, Issue 4, Pages 223-238Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/157340211004150319123313
Keywords
Corticosteroid; collecting duct; epithelial sodium channel; endothelin; nitric oxide
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Funding
- National Institutes of Health Grants [DK76131, HL49277]
- Juvenile Diabetes Research Foundation [2006-2-106]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL049277] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [T32DK007750, U01DK076131] Funding Source: NIH RePORTER
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Although human association studies suggest a link between polymorphisms in the gene encoding transforming growth factor (TGF) beta 1 and differing blood pressure levels, a causative mechanism for this correlation remains elusive. Recently we have generated a series of mice with graded expression of TGF beta 1, ranging from approximately 10% to 300% compared to normal. We have found that blood pressure and plasma volume are negatively regulated by TGF beta 1. Of note, the 10% hypomorph exhibits primary aldosteronism and markedly impaired urinary excretion of water and electrolytes. We here review previous literature highlighting the importance of TGF beta signaling as a natriuretic system, which we postulate is a causative mechanism explaining how polymorphisms in TGF beta 1 could influence blood pressure levels.
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