Atrial natriuretic peptide increases resistance to venous return in rats

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Abstract
To examine mechanisms by which administration of atrial natriuretic peptide (ANP) decreases venous return, we compared the hemodynamic effects of ANP (0.5 .mu.g .cntdot. min-1 .cntdot. kg-1), furosemide (FU, 10 .mu.g .cntdot. min-1 .cntdot. kg-1), and hexamethonium (HEX, 0.5 mg .cntdot. min-1 .cntdot. kg-1) with those of vehicle (VE) in anesthetized rats. Compared with VE, ANP reduced mean arterial pressure (106 .+-. 4 vs. 92 .+-. 3 mmHg; P < 0.05), central venous pressure (0.3 .+-. 0.3 vs. -0.7 .+-. 0.2 mmHg; P < 0.01), and cardiac index (215 .+-. 12 vs. 174 .+-. 10 ml .cntdot. min-1 .cntdot. kg-1; P < 0.05) and increased calculated resistance to venous return (32 .+-. 3 vs. 42 .+-. 2 mmHg .cntdot. ml-1 .cntdot. min .cntdot. g; P < 0.01). Mean circulatory filling pressure, distribution of blood flow between splanchnic organs and skeletal muscles, and total peripheral resistance remained unchanged. FU increased urine output similar to that of ANP, yet produced no hemodynamic changes, dissociating diuresis, and decreased cardiac output. HEX lowered arterial pressure through a reduction in total peripheral resistance without altering cardiac output or resistance to venous return. The results confirm previous findings that ANP decreases cardiac output through a reduction in venous return and suggest that this results partly from increased resistance to venous return and not from venodilation on redistribution of blood flow.

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