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Vasodilation, enhanced vascular permeability, and increased renal excretion of salt and water are at least three of the acute mechanisms through which atrial natriuretic peptide (ANP) reduces plasma volume.
The NPPA gene in humans encodes the natriuretic peptide hormone known as atrial natriuretic peptide (ANP) or atrial natriuretic factor (ANF), which is secreted by the cardiac atria.
In order to discriminate between the effects of ANP-dependent increases in vascular permeability and those of other endocrine actions of ANP in the regulation of plasma volume, authors of a study in this issue of the JCI carried out a knockout of the ANP receptor in vascular endothelia. Reduced vascular permeability to plasma protein was seen in the knockout animals, which led to chronically elevated plasma volume, arterial hypertension, and cardiac hypertrophy.
These modifications were not explained by vasodilation or renal excretion. Thus, ANP's capacity to reduce arterial blood pressure may depend on the extent to which it enhances endothelial permeability.
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