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Background Cardiac atrial natriuretic peptide (ANP) is an essential physiological regulator of arterial blood pressure and intravascular volume. Unlike other “natriuretics”, which reduce interstitial fluid volume with little change in plasma volume, ANP has important extrarenal, endothelial actions that enable it to reduce plasma volume preferentially. Thus ANP, via its guanylyl cyclase-A (GC-A) receptor and cyclic GMP formation, enhances microvascular endothelial permeability to albumin, ultimately moving plasma fluid into interstitial pools. However, the cellular pathways mediating this effect are unknown.v Here we investigated the role of caveolae-mediated endothelial albumin transcytosis in the mechanism of increased permeability induced by ANP.

Atrial natriuretic peptide increases the albumin permeability of mouse skeletal muscle microcirculation by the caveolae-mediated transcellular pathway