1: Am J Physiol. 1992 Mar;262(3 Pt 2):R509-16. 

Captopril enhances renal responsiveness to ANF in dogs with compensated
high-output heart failure.

Villarreal D, Freeman RH, Johnson RA.

Department of Physiology, University of Missouri School of Medicine, Columbia
65212.

The systemic hemodynamic, hormonal, and renal effects of chronic
angiotensin-converting enzyme inhibition (CEI) with captopril and the responses
to synthetic atrial natriuretic factor (ANF) infusions in the presence and
absence of captopril were examined in normal dogs (n = 6) and in dogs with an
arteriovenous (AV) fistula and compensated high-output heart failure (n = 6).
This experimental model is characterized by normalization of the circulating
renin-angiotensin-aldosterone system (RAAS) and persistent elevations in central
filling pressures and plasma ANF. In both normal and AV-fistula dogs, oral
captopril for 1 wk at 35 mg.kg-1.day-1 in three divided doses produced
progressive reductions in arterial and atrial pressures (P less than 0.05),
plasma ANF (P less than 0.05), and aldosterone (P less than 0.05). After 1-2
days of a modest increase in urinary sodium excretion (UNaV) (P less than 0.05),
all of the dogs regained and maintained sodium balance during captopril
administration. On the 8th day of the captopril regimen, synthetic ANF was
infused at 15 and 30 ng.kg-1.min-1 for 75-min periods each. Control infusion
experiments were performed in the same animals before captopril administration.
The normal dogs exhibited dose-related elevations in UNaV (P less than 0.05)
that were not augmented with captopril (P greater than 0.05). In contrast, in
the AV-fistula dogs the observed renal unresponsiveness to synthetic ANF in the
control experiments was reversed with chronic CEI, and ANF-induced UNaV achieved
levels comparable to those obtained in the normal animals.(ABSTRACT TRUNCATED AT
250 WORDS)

PMID: 1313653 [PubMed - indexed for MEDLINE]