Figure 226

Role of renal perfusion pressure in sodium (Na) retention. A, Results from studies in rats that had undergone myocardial infarction (MI) or placement of an arteriovenous fistula (AVF) [54]. Rats with small and large MIs were identified. Both small and large MIs induced significant Na retention when challenged with Na loads. Renal Na retention occurred in the setting of mild hypotension. AVF also induced significant Na retention, which was associated with a decrease in mean arterial pressure (MAP) [55,56]. Figure 2-3 has shown that Na excretion decreases greatly for each mm Hg decrease in MAP. B, Results of two groups of experiments performed by Levy and Allotey [57,58] in which experimental cirrhosis was induced in dogs by sporadic feeding with dimethylnitrosamine. Three cirrhotic stages were identified based on the pattern of Na retention. In the first, dietary Na intake was balanced by Na excretion. In the second, renal Na retention began, but still without evidence of ascites or edema. In the last, ascites were detected. Because Na was retained before the appearance of ascites, "primary" renal Na retention was inferred. An alternative interpretation of these data suggests that the modest decrease in MAP is responsible for Na retention in this model. Note that in both heart failure and cirrhosis, Na retention correlates with a decline in MAP.

FIGURE 2-27

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.

FIGURE 2-28

Mechanism of renal resistance to atrial natriuretic peptide (ANP) in experimental low-output heart failure. Low-output heart failure was induced in dogs by thoracic inferior vena caval constriction (TIVCC), which also led to a significant decrease in renal perfusion pressure (RPP) (from 127 to 120 mm Hg). ANP infusion into dogs with TIVCC did not increase urinary sodium (Na) excretion (ÜNaV, ANP group). In contrast, when the RPP was returned to baseline by infusing angiotensin II (AII), urinary Na excretion increased greatly (ANP + AII). To exclude a direct effect of AII on urinary Na excretion, intrarenal saralasin (SAR) was infused to block renal AII receptors. SAR did not significantly affect the natriuresis induced by ANP plus AII. An independent effect of SAR on urinary Na excretion was excluded by infusing ANP plus SAR and AII plus SAR. These treatments were without effect. These results were interpreted as indicating that the predominant cause of resistance to ANP in dogs with low-output congestive heart failure is a reduction in RPP. (Data from Redfield and coworkers [61].)

Fluid intake

Nonrenal fluid loss M3

Net volume intake

Arterial pressure

Kidney volume output

Kidney volume output

Rate of change of extracellular fluid volume

Total peripheral resistance

^^ Autoregulation

Cardiac output ^

Rate of change of extracellular fluid volume

Venous return

10 20

ECF volume, L

10 20

ECF volume, L

Extracellular fluid volume

Blood volume m:

I Mean circulatory I filling pressure

30 20 10 0

Extracellular fluid volume

Blood volume

0 0

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