Figure 211

Control of systemic hemodynamics by the atrial natriuretic peptide (ANP) system. Increases in atrial stretch (PRELOAD) increase ANP secretion by cardiac atria. The primary amino acid sequence of ANP is shown in single letter code with its disulfide bond indicated by the lines. The amino acids highlighted in blue are conserved between ANP, brain natriuretic peptide, and C-type natriuretic pep-tide. ANP has diverse functions that include but are not limited to the following: stimulating vagal afferent activity, increasing capillary permeability, inhibiting renal sodium (Na) and water reabsorption, inhibiting renin release, and inhibiting arteriolar contraction. These effects reduce sympathetic nervous activity, reduce angiotensin II generation, reduce aldosterone secretion, reduce total peripheral resistance, and shift fluid out of the vasculature into the intersti-tium. The net effect of these actions is to decrease cardiac output, vascular volume, and peripheral resistance, thereby returning preload toward baseline. Many effects of ANP (indicated by solid arrows) are diminished in patients with edematous disorders (there is an apparent resistance to ANP). Effects indicated by dashed arrows may not be diminished in edematous disorders; these effects contribute to shifting fluid from vascular to extravascular tissue, leading to edema. This observation may help explain the association between elevated right-sided filling pressures and the tendency for Na retention [22]. (Modified from Brenner and coworkers [23].)

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