Captopril and hydralazine suppress atrial natriuretic peptide (ANP) gene expression in the ventricles of spontaneously hypertensive rat

Fukui, Kiyoshi; Itoh, Hiroshi; Yamamoto, Akira; Takahashi, Toshiaki; Shoji, Tetsuo; Kimura, Shoji; Aki, Yasuharu; Hasui, Kouichi; Ohkubo, Hiroaki; Nakanishi, Shigetada; Abe, Youichi

doi:10.1016/0006-291x(89)91657-4

Cited by 16 publications

(12 citation statements)

References 17 publications

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“…Treatment with minoxidil produced a 1.6-2.1 fold increase in ventricular ANP mRNA, and plasma IR-ANP levels were significantly elevated when compared to the untreated controls, as shown earlier by Stasch et al (1987a). Hydralazine, another vasodilator, has been shown to have no effect on plasma IR-ANP levels (Oda et al, 1988), and even to decrease ANP mRNA levels (Fukui et al, 1989), but, on the other hand, it did not significantly change cardiac weight either.…”

Section: Chemicalsmentioning

confidence: 53%

“…The calcium antagonists, nitrendipine and nisoldipine reduce the spontaneously developing hypertrophy and decrease the elevated plasma IR-ANP levels (Stasch et al, 1986;1987a, b). Others have demonstrated a decrease both in relative ventricular weight and in plasma IR-ANP after chronic treatment with a calcium antagonist (Kohno et al, 1988) or angiotensin I converting-enzyme inhibitors (Kohno et al, 1987;Oda et al, 1988;Fukui et al, 1989). Minoxidil treatment, in turn, aggravated cardiac hypertrophy and produced an additional increase in plasma IR-ANP (Stasch et al, 1987a).…”

Section: Chemicalsmentioning

confidence: 99%

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Release of atrial natriuretic peptide from rat myocardium in vitro: effect of minoxidil‐induced hypertrophy

Kinnunen

Taskinen

Leppäluoto

et al. 1990

British J Pharmacology

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1 Ventricular hypertrophy is characterized by stimulation of ventricular synthesis of atrial natriuretic peptide (ANP). To examine the role of ventricular ANP levels in the secretion of ANP into the circulation, atrial and ventricular levels of immunoreactive-ANP (IR-ANP) as well as ANP messenger RNA (mRNA), and the release of IR-ANP from isolated perfused hearts, both before and after atrialectomy, were measured simultaneously in control and minoxidil-treated Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. 2 IR-ANP levels in the ventricles of untreated, 12 month-old SHR with severe ventricular hypertrophy were increased when compared to age-matched WKY rats. Minoxidil treatment for 8 weeks in both strains resulted in a decrease in mean arterial pressure and increases in ventricular weight to body weight ratios, plasma IR-ANP concentrations (in WKY from 133 + 20 to 281 + 34pgml-1, P < 0.01; in SHR from 184 + 38 to 339 + 61 pgml-', P < 0.05), and in ventricular IR-ANP contents (in WKY: 53%; in SHR: 41%). A highly significant correlation was found between ventricular IR-ANP content and ventricular weight to body weight ratio (r = 0.59, P < 0.001, n = 26). 3 When studied in vitro, in isolated perfused heart preparations, the hypertrophied ventricular tissue after atrialectomy secreted more ANP into the perfusate than ventricles of the control hearts; ventricles contributed 28%, 22%, 18% and 15% of the total ANP release to perfusate in the minoxidil-treated SHR, control SHR, minoxidil-treated WKY and control WKY, respectively. A significant correlation was found between the IR-ANP release from ventricles and ventricular weight to body weight ratio (r = 0.56, P < 0.01, n = 24). 4 These studies demonstrate that the ventricles contribute substantially to the circulating level of ANP, and that the amount released depends on the degree of ventricular hypertrophy.

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Section: Chemicalsmentioning

confidence: 53%

Section: Chemicalsmentioning

confidence: 99%

Release of atrial natriuretic peptide from rat myocardium in vitro: effect of minoxidil‐induced hypertrophy

Kinnunen

Taskinen

Leppäluoto

et al. 1990

British J Pharmacology

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“…Augmented expression of these peptides in both chambers of SHR may therefore reflect sensitivity of these genes to the regulatory influence of pressure loading since modest pressure loading is also evident in the right ventricle of SHR [20]. Normalisation of systemic blood pressure in SHR attenuates augmented expression of ANP and BNP in the heart [19]. In contrast, blood pressure normalisation in rats subjected to chronic nitric oxide deficiency does not attenuate the augmented expression of IMD observed in both ventricles in that model [10].…”

Section: Discussionmentioning

confidence: 97%

“…Augmented expression in SHR hearts of the natriuretic peptides, ANP and BNP, which offset increased cardiac preload and after-load by promoting natriuresis, diuresis and vasodilatation [18] is normalised by blood pressure lowering [19]. Modest pulmonary hypertension is also present in SHR at 20 weeks [20] but right ventricular hypertrophy (RVH) is not evident in non-failing SHR hearts [21].…”

Section: Introductionmentioning

confidence: 99%

Expression of the Counter-Regulatory Peptide Intermedin is Augmented in the Presence of Oxidative Stress in Hypertrophied Cardiomyocytes

Bell

Zhao²,

McCoy³

et al. 2008

Cell Physiol Biochem

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Background: Intermedin (IMD), a novel cardiac peptide related to adrenomedullin (AM), protects against myocardial ischemia-reperfusion injury and attenuates ventricular remodelling. IMD’s actions are mediated by a calcitonin receptor-like receptor in association with receptor activity modifying proteins (RAMPs 1-3). Aim/method: using the spontaneously hypertensive rat (SHR) and normotensive Wistar Kyoto (WKY) rat at 20 weeks of age, to examine (i) the presence of myocardial oxidative stress and concentric hypertrophy; (ii) expression of IMD, AM and receptor components. Results: In left and right ventricular cardiomyocytes from SHR vs. WKY cell width (26% left, 15% right) and mRNA expression of hypertrophic markers ANP (2.7 fold left, 2.7 fold right) and BNP (2.2 fold left, 2.0 fold right) were enhanced. In left ventricular cardiomyocytes only (i) oxidative stress was indicated by increased membrane protein carbonyl content (71%) and augmented production of O_2- anion (64%); (ii) IMD (6.8 fold), RAMP1 (2.5 fold) and RAMP3 (2.0 fold) mRNA was increased while AM and RAMP2 mRNA was not altered; (iii) abundance of RAMP1 (by 48%), RAMP2 (by 41%) and RAMP3 (by 90%) monomers in cell membranes was decreased. Conclusion: robust augmentation of IMD expression in hypertrophied left ventricular cardiomyocytes indicates a prominent role for this counter-regulatory peptide in the adaptation of the SHR myocardium to the stresses imposed by chronic hypertension. The local concentration and action of IMD may be further enhanced by down-regulation of NEP within the left ventricle.

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“…The amounts of total RNA obtained per gram of each tissue were 0.96 ± 0.06 mg. Quantitative measurement of ANP mRNA was performed by Northern blot hy bridization analysis as previously reported (17). In short, total RNA was denatured with 1 M glyoxal and 50% dimethylsulfoxide, elec trophoresed on 1.5% agarose gels, and trans ferred to Biodyne A membranes (Pall Ultra fine Filtration Corp., Glen Cove, NY, U.S.A).…”

Section: Methodsmentioning

confidence: 99%

Effects of Water Deprivation and Morphine Administration on Atrial Natriuretic Peptide mRNA Levels in Rat Auricles

Fukui

Itoh

Takahashi

et al. 1991

Japanese Journal of Pharmacology

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We investigated the influences of two potent stimuli, water deprivation (5 days) and morphine administration (100 mg/kg), on the level of atrial natriuretic peptide (ANP) mRNA in the rat auricles. The ANP mRNA level was measured by Northern blot hybridization analysis. The plasma concentration of ANP decreased in water deprived rats, and the ANP mRNA levels in both auricles of these rats were lower than those of the control, particularly in the left auricle. Thirty minutes after the injection of morphine, the plasma concentration of ANP markedly increased, while morphine increased the right auricular ANP mRNA level 4 hr after the adminis tration. These data suggest that these stimuli can change ANP gene expression in the auricles and that the changes are induced differentially in both auricles.

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Captopril and hydralazine suppress atrial natriuretic peptide (ANP) gene expression in the ventricles of spontaneously hypertensive rat

Cited by 16 publications

References 17 publications

Release of atrial natriuretic peptide from rat myocardium in vitro: effect of minoxidil‐induced hypertrophy

Release of atrial natriuretic peptide from rat myocardium in vitro: effect of minoxidil‐induced hypertrophy

Expression of the Counter-Regulatory Peptide Intermedin is Augmented in the Presence of Oxidative Stress in Hypertrophied Cardiomyocytes

Effects of Water Deprivation and Morphine Administration on Atrial Natriuretic Peptide mRNA Levels in Rat Auricles

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