Although human association studies suggest a link between polymorphisms in the gene encoding transforming
growth factor (TGF) β1 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 TGFβ1, ranging from approximately 10% to 300%
compared to normal. We have found that blood pressure and plasma volume are negatively regulated by TGFβ1. 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 TGFβ signaling as a natriuretic system, which we
postulate is a causative mechanism explaining how polymorphisms in TGFβ1 could influence blood pressure levels.
Keywords: Corticosteroid, collecting duct, epithelial sodium channel, endothelin, nitric oxide.
Rights & PermissionsPrintExport