Rockville, Md. (April 27, 2022)—A new study finds male and female mice with a novel mutation in the protein cullin3 that causes deletion of the coding region exon-9 developed salt-induced high blood pressure and renal injury. The effect of salt was greater in female mice, according to a new study published ahead of print in the journal Function. The new findings show “[Cullin3 mutations in the endothelium may contribute to human hypertension in part through decreased endothelial [nitric oxide] bioavailability, renovascular dysfunction and increased salt-sensitivity of blood pressure,” according to the researchers. This model recapitulates the greater salt sensitivity of blood pressure in women than in men and may be useful to study the human phenotype.
Read the full article, “Endothelial cullin3 mutation impairs nitric oxide-mediated vasodilation and promotes salt-induced hypertension,” published ahead of print in Function. Contact APS Media Relations or call 301.634.7314 to schedule an interview with a member of the research team.
