Figure 228

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 (UNaV, 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

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