Figure 227

Mechanism of sodium (Na) retention in high-output cardiac failure. Effects of high-output heart failure induced in dogs by arteriovenous (AV) fistula [59]. After induction of an AV fistula (day 0), plasma renin activity (PRA; thick solid line) increased greatly, correlating temporally with a reduction in urinary Na excretion (UNaV; thin solid line). During this period, mean arterial pressure (MAP; dotted line) declined modestly. After day 5, the plasma atrial natriuretic peptide concentration (ANP; dashed line) increased because of volume expansion, returning urinary Na excretion to baseline levels. Thus, Na retention, mediated in part by the renin-angiotensin-aldos-terone system, led to volume expansion. The volume expansion suppressed the renin-angiotensin-aldosterone system and stimulated ANP secretion, thereby returning Na excretion to normal. These experiments suggest that ANP secretion plays an important role in maintaining Na excretion in compensated congestive heart failure. This effect of ANP has been confirmed directly in experiments using anti-ANP antibodies [60]. AI—angiotensin I.

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