Angiotensin converting enzyme inhibition restores cardiac and hormonal responses to volume overload in patients with dilated cardiomyopathy and mild heart failure.

Volpe, Massimo; Tritto, C; DeLuca, N.; Rubattu, Speranza; Mele, Alessandro F.; Lembo, Giuseppe; Enea, Iolanda; deCampora, Paolo; Rendina, Virgilio; Romanò, Massimo

doi:10.1161/01.cir.86.6.1800

Cited by 35 publications

(20 citation statements)

References 42 publications

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“…However, the ANP response to acute volume expansion is blunted in cardiac hypertrophy as well as heart failure (18,23,25). It is unclear whether the impaired ANP release in heart failure is a result of neurohormonal suppression or due to an inhibition of the release mechanism itself.…”

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confidence: 99%

Rat corin gene: molecular cloning and reduced expression in experimental heart failure

Langenickel¹,

Pagel²,

Buttgereit³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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Stored cardiac pro-atrial natriuretic peptide (pro-ANP) is converted to ANP and released upon stretch from the atria into the circulation. Corin is a serin protease with pro-ANP-converting properties and may be the rate-limiting enzyme in ANP release. This study was aimed to clone and sequence corin in the rat and to analyze corin mRNA expression in heart failure when ANP release upon stretch is blunted. Full-length cDNA of rat corin was obtained from atrial RNA by RT-PCR and sequenced. Tissue distribution as well as regulation of corin mRNA expression in the atria were determined by RT-PCR and RNase protection assay. Heart failure was induced by an infrarenal aortocaval shunt. Stretch was applied to the left atrium in a working heart modus, and ANP was measured in the perfusates. The sequence of rat corin cDNA was found to be 93.6% homologous to mouse corin cDNA. Corin mRNA was expressed almost exclusively in the heart with highest concentrations in both atria. The aortocaval shunt led to cardiac hypertrophy and heart failure. Stretch-induced ANP release was blunted in shunt animals (control 1,195 +/- 197 fmol.min(-1).g(-1); shunt: 639 +/- 99 fmol.min(-1).g(-1), P < 0.05). Corin mRNA expression was decreased in both atria in shunt animals [right atrium: control 0.638 +/- 0.004 arbitrary units (AU), shunt 0.566 +/- 0.014 AU, P < 0.001; left atrium: control 0.564 +/- 0.009 AU, shunt 0.464 +/- 0.009 AU, P < 0.001]. Downregulation of atrial corin mRNA expression may be a novel mechanism for the blunted ANP release in heart failure.

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confidence: 99%

Rat corin gene: molecular cloning and reduced expression in experimental heart failure

Langenickel¹,

Pagel²,

Buttgereit³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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“…Indeed, the impaired ability to excrete ingested sodium is a key feature of patients with congestive HF [4,5]. Recent studies have demonstrated that renal sodium retention can occur in patients with asymptomatic LVD and mild HF [6][7][8], and in experimental HF, without increased activation of the RAAS [14]. It is difficult to elucidate mechanisms by which sodium and water retention occur in very early heart disease as most patients immediately receive (or have already received) treatment that affects the mechanisms being studied.…”

Section: Discussionmentioning

confidence: 99%

“…Despite this, the pathophysiology of sodium and water retention in HF, particularly with regard to the time of onset of this abnormality during the course of the disease, remains inadequately studied. Volpe and co-workers [6][7][8] have reported that patients with asymptomatic LVD or mild HF clearly show abnormalities in renal sodium and water handling well before detectable changes in cardiac output. However, few studies have examined the response to chronic volume loading immediately post-MI.…”

Section: Introductionmentioning

confidence: 99%

Natriuretic peptides maintain sodium homoeostasis during chronic volume loading post-myocardial infarction in sheep

Charles¹,

Elliott²,

Nicholls³

et al. 2003

Clinical Science

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The impaired ability to excrete sodium is a key feature of established congestive heart failure and is also apparent in asymptomatic left ventricular (LV) impairment. However, few studies have examined responses to chronic volume loading immediately post-myocardial infarction (MI). Experimental MI was induced in six sheep by thrombogenic coil coronary artery occlusion, and resulted in significant LV dysfunction with reduced LV ejection fraction ( P =0.001) and subsequent remodelling (increased LV volumes, P =0.015). Chronic volume loading with 2, 3 and 4 litres/day intravenous saline (each for 7 days) showed no evidence of renal sodium or volume retention in sheep with experimental MI compared with six normal control sheep. Plasma levels of brain natriuretic peptide (BNP), N-terminal pro-BNP and cGMP (all P <0.05) were higher in the MI group compared with normal control sheep. There were no differences in haemodynamics, body mass or renin-aldosterone levels between groups. This study provides evidence that natriuretic peptides play a pivotal role in preserving volume/electrolyte balance in the early stages of post-MI cardiac dysfunction.

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“…In chronic heart failure, sympathetic activity is usually increased, causing systemic vasoconstriction via vascular c~-adrenoceptor and maintaining cardiac output via myocardial/~-receptors [8]. The preload reserve is also greatly limited in the failing heart [9]. In the presence of these abnormalities, a selective decrease in heart rate and cardiac contractility due to myocardial/~-receptor blockade could disclose a state of afterload mismatch, further decreasing cardiac output.…”

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confidence: 99%

Pharmacological effects of concomitant administration of ?-adrenoceptor blocker and agonist in normal subjects: characterization by heart rate response to exercise

Karita

Sato

Koretsune

et al. 1995

Eur J Clin Pharmacol

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The effects of a combination regimen of metoprolol and beta 1-adrenoceptor agonist denopamine on resting and exercise heart rate have been studied in 10 normal volunteers. Maximal ramp upright bicycle exercise was performed three times at 1-week intervals. Two hours before each exercise test, 5 mg metoprolol plus 20 mg denopamine, 5 mg metoprolol plus a denopamine placebo, or two placebos were orally administered in a double-blind fashion. During exercise after placebo administration, heart rate increased in parallel with the exercise intensity. Compared to the placebo values, resting heart rate was significantly decreased by an average of 10 beats.min-1 by 5 mg metoprolol, whereas it was not altered by the combination regimen. During exercise, however, both the combination regimen and metoprolol alone showed a significant negative chronotropic effect, decreasing peak exercise heart rate by an average of 14 and 21 beats.min-1, respectively. Peak oxygen uptake was also significantly decreased by both regimens. We conclude that concomitant administration of 5 mg metoprolol and 20 mg denopamine exerts an effective beta-adrenoceptor blocking action during exercise but a minimal effect at rest in normal subjects. The combination regimen appears to have a favourable pharmacological profile for beta-adrenoceptor blocker therapy in patients with chronic heart failure.

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Angiotensin converting enzyme inhibition restores cardiac and hormonal responses to volume overload in patients with dilated cardiomyopathy and mild heart failure.

Cited by 35 publications

References 42 publications

Rat corin gene: molecular cloning and reduced expression in experimental heart failure

Rat corin gene: molecular cloning and reduced expression in experimental heart failure

Natriuretic peptides maintain sodium homoeostasis during chronic volume loading post-myocardial infarction in sheep

Pharmacological effects of concomitant administration of ?-adrenoceptor blocker and agonist in normal subjects: characterization by heart rate response to exercise

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