Faculty Research 1990 - 1999

Title

Genetic decreases in atrial natriuretic peptide and salt-sensitive hypertension [published erratum appears in Science 1995 Mar 24;267(5205):1753]

Document Type

Article

Publication Date

1995

Keywords

Atrial-Natriuretic-Factor: an, bl, ge, df, Blood-Pressure, Crosses-Genetic, Female, Gene-Targeting, Genotype, Heart-Atrium: ul, Heterozygote, Homozygote, Hypertension: ge, pp, pa, Male, Mice, Mice-Inbred-C57BL, Protein-Precursors: ge, Sodium-Dietary, SUPPORT-NON-U-S-GOVT, SUPPORT-U-S-GOVT-P-H-S

JAX Source

Science 1995 Feb 3;267(5198):679-81

Grant

GM20069/GM/NIGMS, HL49277/HL/NHLBI

Abstract

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.

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