Effect of converting-enzyme inhibition on renal response to ANF in rats with experimental heart failure

Abassi, Zaid; Haramati, Aviad; Hoffman, A.; Burnett, J. C.; Winaver, Joseph

doi:10.1152/ajpregu.1990.259.1.r84

Cited by 32 publications

(42 citation statements)

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“…Importantly, the potentiating action oflow dose inhibition ofAll generation occurred despite a tendency towards reduced renal perfusion pressure, a parameter of profound functional importance for renal responses to ANF (5). Analogously, Abassi et al (17) demonstrated that CEI potentiated natriuretic responses to ANF in CHF despite significant decreases in renal perfusion pressure. Moreover, the observation that chronic inhibition of All generation did not significantly alter systemic hemodynamics at baseline compared with untreated CHF suggests that potentiation of NEP-I action was not simply a consequence of reducing the hemodynamic severity of CHF.…”

Section: Discussionmentioning

confidence: 89%

“…Studies by Appel et al (32) demonstrate that ANF, and its intracellular second messenger cGMP, dose-dependently antagonize AII-mediated mesangial cell contraction. In addition, Showalter et al ( 16) observed that low dose intrarenal All attenuates ANF-mediated changes in both GFR and tubular sodium reabsorption in the normal dog, while the studies of Abassi et al (17) indicate that CEI restores tubular responses to ANF in rats with CHF. Studies by Salazar et al (33) suggest that All antagonizes ANF induced decreases in proximal tubule reabsorption.…”

Section: Discussionmentioning

confidence: 99%

“…In fact, previous studies have demonstrated antagonism between the RAAS and ANF with respect to both renal hemodynamics and tubular sodium handling (16,17). In general, ANF promotes sodium excretion and vasorelaxation while angiotensin II (All) promotes sodium retention and vasoconstriction.…”

Section: Introductionmentioning

confidence: 99%

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Angiotensin inhibition potentiates the renal responses to neutral endopeptidase inhibition in dogs with congestive heart failure.

et al. 1991

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The renal natriuretic actions of endogenous atrial natriuretic factor are enhanced by neutral endopeptidase inhibition (NEP-I). Recognizing that activation ofthe renin-angiotensin-aldosterone system in congestive heart failure (CHF) antagonizes the renal actions of atrial natriuretic factor, we hypothesized that angiotensin II antagonism with converting enzyme inhibition would potentiate the renal actions of NEP-I in CHF. To test this hypothesis, the renal responses to a specific NEP-I (SQ 28,603) were assessed in dogs with eight days of experimental CHF produced by rapid ventricular pacing. The renal natriuretic responses to NEP-I in experimental CHF were significant. In the same model of CHF, chronic angiotensin antagonism with converting enzyme inhibition potentiated both renal hemodynamic and excretory responses to NEP-I. The potentiated renal hemodynamic response included significant increases in glomerular filtration rate and filtration fraction. In the CHF group with angiotensin antagonism, an intrarenal infusion of low-dose angiotensin abolished the potentiated renal responses to NEP-I, supporting the concept that intrarenal angiotensin antagonism, rather than improved systemic hemodynamics or potentiation of other peptide systems, mediated the enhanced renal responses to NEP-I in the presence of converting enzyme inhibition. (J. Clin. Invest. 1991. 88:1636-1642

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Section: Discussionmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 99%

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Angiotensin inhibition potentiates the renal responses to neutral endopeptidase inhibition in dogs with congestive heart failure.

et al. 1991

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“…Chronic inhibition of angiotensin-converting enzyme (ACE), to reduce angiotensin II production, has been shown to improve the natriuretic response to ANP in animal models of cardiac failure (Raya et al, 1989;Abassi et al, 1990;Villarreal et al, 1992). This has prompted interest in the effect of ACE inhibitors on the response to E-24.11 inhibition and the possibility of synthesizing dual inhibitors i.e.…”

Section: Introductionmentioning

confidence: 99%

Renal effects of concurrent E‐24.11 and ACE inhibition in the aorto‐venocaval fistula rat

Kirk¹,

Wilkins²

1996

British J Pharmacology

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1 The present studies compare the early renal response to (a) an endopeptidase-24.11 (E-24.11) inhibitor (candoxatrilat) (b) an angiotensin-converting enzyme (ACE) inhibitor (lisinopril) and (c) the combination of endopeptidase-24.11 and ACE inhibition in the rat A-V fistula model of chronic volume overload. 2 Candoxatrilat (3 and 10 mg kg-') i.v. produced a prompt 3 fold increase in urinary sodium and cyclic GMP excretion without affecting significantly blood pressure or glomerular filtration rate (GFR).3 Lisinopril (0.03 mg kg-') alone inhibited the pressor response to angiotensin I but had no significant effect on urinary sodium excretion or blood pressure.4 Lisinopril (0.03 mg kg-') attenuated significantly the early natriuretic response to candoxatrilat (3 mg kg-1) and the associated rise in urinary cyclic GMP, but sodium excretion eventually reached levels associated with acute E-24.11 inhibition. 5 Doses of the dual E-24. 11/ACE inhibitor, sampatrilat, that inhibited the pressor response to angiotensin I reduced mean arterial blood pressure and produced a delayed natriuresis and rise in urinary cyclic GMP excretion when compared to candoxatrilat alone. 6 Concurrent administration of an ACE inhibitor reduces the early renal response to E-24.11 inhibition in the A-V fistula rat, an effect attributable to the hypotensive action of this combination.

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“…Clinical and experimental data provide strong evidence that this axis is involved in the pathogenesis of the cardiac, renal, and vascular changes of CHF and hypertension (2,4,7,12,14,35,37). Moreover, inhibitors of angiotensin-converting enzyme (ACE) have been found to be highly beneficial in the treatment of patients with CHF (2, 4, 31a, 31b, 37).…”

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confidence: 99%

Cardiac and renal effects of omapatrilat, a vasopeptidase inhibitor, in rats with experimental congestive heart failure

Abassi

Yahia²,

Zeid³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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. Cardiac and renal effects of omapatrilat, a vasopeptidase inhibitor, in rats with experimental congestive heart failure. Am J Physiol Heart Circ Physiol 288: H722-H728, 2005. First published October 21, 2004 doi:10.1152/ ajpheart.00737.2004 is a novel mixed inhibitor of angiotensin-converting enzyme (ACE) and neutral endopeptidase 24.11 (NEP), the enzyme that metabolizes natriuretic peptides. Congestive heart failure (CHF) is characterized by excessive sodium retention, attributed to both an excessive effect of angiotensin II and diminished responsiveness to natriuretic peptides. In this study, we examined the acute and chronic renal and cardiac effects of OMP in rats with compensated [urinary sodium excretion (U NaV) Ͼ 1,200 eq/day] and decompensated (U NaV Ͻ 100 eq/day) CHF, induced by a surgical aortocaval fistula (ACF). Bolus injection of OMP (10 mg/kg) to sham controls produced significant diuretic and natriuretic responses [U NaV increased from 0.67 Ϯ 0.19 to 3.27 Ϯ 1.35 eq/min, P Ͻ 0.05; fractional sodium excretion (FE Na) increased from 0.23 Ϯ 0.06 to 0.95 Ϯ 0.34%, P Ͻ 0.01] despite a significant decline in blood pressure (BP). Rats with compensated CHF displayed blunted diuresis and natriuresis to this dose of OMP but a significant decrease in BP. However, in rats with decompensated CHF, OMP induced significant natriuresis (FE Na increased from 0.18 Ϯ 0.15 to 0.82 Ϯ 0.26%, P Ͻ 0.05) despite a further decrease in BP (from 90 Ϯ 9 to 71 Ϯ 6 mmHg, P Ͻ 0.01). Two weeks after ACF, the heart/body weight ratio was significantly greater in rats with CHF than controls (0.51 Ϯ 0.026 vs. 0.30 Ϯ 0.004%, P Ͻ 0.0001), and U NaV was significantly lower. Immediate or late (1 or 6 days after ACF) OMP treatment in the drinking water (140 mg/l) reduced cardiac hypertrophy to 0.41-0.43% (P Ͻ 0.01) and induced natriuresis. These results suggest that OMP improves both sodium balance and cardiac remodeling and might be advantageous to ACE inhibitors for the treatment of decompensated CHF. cardiac hypertrophy; renal function; rat; angiotensin-converting enzyme inhibitor; neutral endopeptide inhibitor

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Effect of converting-enzyme inhibition on renal response to ANF in rats with experimental heart failure

Cited by 32 publications

References 0 publications

Angiotensin inhibition potentiates the renal responses to neutral endopeptidase inhibition in dogs with congestive heart failure.

Angiotensin inhibition potentiates the renal responses to neutral endopeptidase inhibition in dogs with congestive heart failure.

Renal effects of concurrent E‐24.11 and ACE inhibition in the aorto‐venocaval fistula rat

Cardiac and renal effects of omapatrilat, a vasopeptidase inhibitor, in rats with experimental congestive heart failure

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