Genetic decreases in atrial natriuretic peptide and salt-sensitive hypertension

Science. 1995 Feb 3;267(5198):679-81. doi: 10.1126/science.7839143.


To determine if defects in the atrial natriuretic peptide (ANP) system can cause hypertension, mice were generated with a disruption of the proANP gene. Homozygous mutants had no circulating or atrial ANP, and their blood pressures were elevated by 8 to 23 millimeters of mercury when they were fed standard (0.5 percent sodium chloride) and intermediate (2 percent sodium chloride) salt diets. On standard salt diets, heterozygotes had normal amounts of circulating ANP and normal blood pressures. However, on high (8 percent sodium chloride) salt diets they were hypertensive, with blood pressures elevated by 27 millimeters of mercury. These results demonstrate that genetically reduced production of ANP can lead to salt-sensitive hypertension.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Atrial Natriuretic Factor / analysis
  • Atrial Natriuretic Factor / blood
  • Atrial Natriuretic Factor / deficiency*
  • Atrial Natriuretic Factor / genetics*
  • Blood Pressure*
  • Crosses, Genetic
  • Female
  • Gene Targeting
  • Genotype
  • Heart Atria / chemistry
  • Heart Atria / ultrastructure
  • Heterozygote
  • Homozygote
  • Hypertension / genetics
  • Hypertension / pathology
  • Hypertension / physiopathology*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Protein Precursors / genetics*
  • Sodium, Dietary / administration & dosage*


  • Protein Precursors
  • Sodium, Dietary
  • Atrial Natriuretic Factor