Alignment of Rat Cardionatrin Sequences with the Preprocardionatrin Sequence from Complementary DNA

Flynn, T. Geoffrey; Davies, P L; Kennedy, B P; Bold, M. de; Bold, A. de

doi:10.1126/science.3157217

Cited by 115 publications

(33 citation statements)

References 27 publications

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“…2 Briefly, RNA samples were reverse transcribed with Super Script II RNase H Ϫ Reverse Transcriptase and oligo(dT) [12][13][14][15][16][17][18] primer with the use of a reverse transcription kit (GIBCO BRL). An aliquot of the cDNA product was used for PCR amplification with ANF primers.…”

Section: Quantitative Competitive Reverse Transcription Polymerase Chmentioning

confidence: 99%

Variable Renal Atrial Natriuretic Factor Gene Expression in Hypertension

et al. 1999

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Abstract-We have previously established the existence of atrial natriuretic factor (ANF) gene expression within the renal parenchyma. Neither the role nor the regulation of this extracardiac source of ANF is clearly defined. To determine whether renal ANF gene expression, similar to cardiac expression, is linked to the activity of the renin-angiotensin system (RAS), we compared renal ANF gene expression in rats after suprarenal aortic banding, a hypertension model associated with activation of RAS, and in the deoxycorticosterone acetate (DOCA)-salt model, which is characterized by depression of RAS. Renal ANF mRNA was measured with a quantitative competitive reverse transcription polymerase chain reaction method. DOCA-salt hypertension significantly reduced the expression of renal ANF. In contrast, aortic banding significantly increased renal ANF expression. In both cases, ANF gene expression in the heart increased. Ramipril treatment at 10 g/kg of aortic-banded rats, a treatment that specifically affects local RAS but maintains hypertension, normalized renal ANF mRNA levels. Altogether, these results suggest that renal ANF gene expression is modulated by local RAS and is independent of circulating RAS and hypertension per se. The marked decrease of renal ANF mRNA in DOCA-salt hypertension suggests a pathogenic role for renal ANF gene downregulation by decreasing the sodium excretory mechanism mediated by the local expression of ANF acting on receptors found in the inner medullary collecting ducts. In aortic banding, renal ANF gene expression upregulation suggests a local compensatory function consistent with the consensus role of natriuretic peptides in the modulation of RAS, thus ameliorating the sodium-retaining effects of renal underperfusion. (Hypertension. 1999;33:1342-1347.)Key Words: atrial natriuretic factor Ⅲ renin-angiotensin system Ⅲ kidney Ⅲ deoxycorticosterone Ⅲ hypertension, renal T he polypeptide hormone atrial natriuretic factor (ANF) plays a significant role in modulating blood volume and blood pressure through cGMP-mediated actions on several target organs. 1 ANF is mainly of atrial origin, but it is also synthesized in other tissues, including the renal parenchyma. 2 Recently, we succeeded in reliably measuring ANF mRNA levels in kidney using a quantitative competitive reverse transcription polymerase chain reaction (QC-RT-PCR) and found that 1 week of deoxycorticosterone acetate (DOCA)-salt administration to rats, a treatment known to increase atrial ANF gene expression without modifying blood pressure, 3 resulted in a significant decrease in renal ANF gene expression. 2 Neither the role nor the regulation of this extracardiac source of ANF is known.Because the renin-angiotensin system (RAS) and ANF often play counterregulatory roles, we took advantage of the known inhibiting effect of the DOCA-salt treatment on RAS on the one hand and the upregulation of RAS after aortic banding on the other to substantiate the hypothesis that renal ANF gene expression may be influenced by RAS status. Furth...

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Section: Quantitative Competitive Reverse Transcription Polymerase Chmentioning

confidence: 99%

Variable Renal Atrial Natriuretic Factor Gene Expression in Hypertension

et al. 1999

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“…For the RNA dot blot analysis, 1 pg and 20ug samples of the RNA from atria and ventricles, respectively, were transferred to a nitrocellulose membrane (Kinnunen et al, 1990). The fulllength rat ANP cDNA probe Car-55 (Flynn et al, 1985) antiserum in the final dilution of 1:25.000 (Vuolteenaho et al, 1985). Synthetic rat ANP1-28, ranging from 0-500 pg per tube, was incubated as standard.…”

Section: Preparation Of Tissuesmentioning

confidence: 99%

Effect of phorbol ester on the release of atrial natriuretic peptide from the hypertrophied rat myocardium

Kinnunen¹,

Taskinen²,

Järvinen³

et al. 1991

British J Pharmacology

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1 To determine the cellular mechanisms of atrial natriuretic peptide (ANP) release from ventricular cardiomyocytes, the secretory and the cardiac effects of a phorbol ester, 12-0-tetradecanoyl-phorbol-13-acetate (TPA), known to stimulate protein kinase C activity in heart cells, were studied in isolated, perfused heart preparations from 2-and 21-month-old Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. TPA was added to the perfusion fluid for 30 min at a concentration of 46 nm after removal of atrial tissue. Additionally, atrial and ventricular levels of immunoreactive ANP (IR-ANP) and ANP mRNA, the distribution of ANP within ventricles as well as the relative contribution of atria and ventricles in the release of ANP were studied. 2 Ventricular hypertrophy that gradually developed in hypertensive rats resulted in remarkable augmentation of ANP gene expression, as reflected by elevated levels of immunoreactive ANP and ANP mRNA. The total amount of IR-ANP in the ventricles of the SHR rats increased 41 fold and ANP mRNA levels 12.9 fold from the age of 2 to 21 months. At the age of 21 months, levels of IR-ANP and ANP mRNA in the ventricles of SHR rats were 5.4 fold and 3.7 fold higher, respectively, than in the normotensive WKY rats. Immunohistochemical studies demonstrated ANP granules within the hypertrophic ventricles of the old SHR rats, but not within normal ventricular tissue. 3 In isolated perfused heart preparations, the severely hypertrophied ventricular tissue of SHR rats after atrialectomy secreted more ANP into the perfusate than did the control hearts. The phorbol ester TPA caused a marked vasoconstriction in both the 2-month and 21-month old normal and hypertrophied hearts. Interestingly, the ANP release from the hypertrophied ventricles of the old SHR rats increased considerably (from 413 + 30 to the maximum of 623 + 75 pgml-1, F = 10.8, P < 0.001, two-way analysis of variance), whereas only a small increase was seen in old WKY rats and no effect was observed in young animals of either strain. When intact rat hearts (without atrialectomy) were used, infusion of phorbol ester also increased the ANP secretion into the perfusate in young animals. 4 Our present results indicate that the phorbol ester TPA increases the release of ANP from the hypertrophied, but not from normal rat myocardium. Thus, hypertrophied rat ventricular myocytes appear to possess the cellular mechanisms necessary to secrete ANP by a regulated pathway. The results further suggest that protein kinase C activity may be involved in the the regulation of ANP secretion from ventricular cells, as has been shown earlier for atrial myocytes.

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“…30 The prehybridization and hybridization solutions for these oligonucleotides consisted of 5 ϫ Denhart's, 6 ϫ SSC, 50 mmol/L monosodium phosphate, 0.5% SDS, and 0.2 mg/mL sssDNA (shared single strand DNA). After 3 h at 60°C for ␣MHC and 52°C for ␤MHC, the membranes were hybridized at the same temperatures for 18 -20 h. The following cDNA probes were used: a) a 900-bp EcoRI/HindIII ANF fragment obtained in our laboratory 31,32 ; b) a 595-bp SalI fragment from BNP cDNA 33 ; c) a 5-kb EcoRI/SalI fragment of the mouse 28S rRNA cDNA 33 ; and d) a 2-kb BamHI/BglII fragment of the mouse phosphoglycerate kinase (PGK) gene cDNA. 30 The Megaprime and the 5Ј-end labeling kits available from Amersham were used to label the cDNA and oligonucleotides, respectively.…”

Section: Total Rna Extraction and Hybridization Proceduresmentioning

confidence: 99%

Atrial natriuretic factor and brain natriuretic peptide gene expression in the spontaneous hypertensive rat during postnatal development

Bold

1998

American Journal of Hypertension

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The increase in natriuretic peptides (NP), atrial natriuretic factor (ANF), and brain natriuretic peptide (BNP) production and release by cardiocytes that occurs in hypertension has been considered to be a compensatory mechanism against ventricular overload. Studies on NP production in the spontaneously hypertensive rat (SHR), an experimental model of human hypertension, have produced controversial results and were carried out when hypertension was already established (> > 17 weeks). At this time, agerelated physiologic and molecular changes in cardiac muscle are difficult to separate from those related to hypertension, ie, increased ANF production and plasma levels. In addition, most of the studies used male rats because the rate of increase in arterial blood pressure-as well as the level to which it rises-is greater in males than in females. Studies of a similar nature using female SHR are not available. The aim of this work was to determine 1) whether ANF and BNP production and secretion increase with the development of hypertension in genetically hypertensive rats; 2) whether a sexual dimorphism in ANF and BNP production and secretion is present in the genetically hypertensive rat during the development of hypertension; and 3) whether the demand for ANF and BNP is the same from each chamber of the heart under these experimental conditions. Age-matched male and female SHR, Wistar-Kyoto (WKY), and Sprague Dawley (SD) rats at 2, 4, and 8 weeks of age were used. The normotensive SD were included to provide a wider basis for baseline findings, as WKY rats are not always a suitable control for SHR due to genetic variations. Natriuretic peptide plasma levels and tissue content were measured by radioimmunoassay. ANF, BNP, as well as ␣-and ␤-myosin heavy chain (MHC) mRNA were estimated by Northern blot analysis. Blood pressure (BP) of more than 150 mm Hg was found only in 8-week-old male SHR. Plasma immunoreactive (ir)ANF and irBNP increased significantly at puberty (8 weeks) in both male and female SHR. The earliest molecular change encountered during the development of hypertension was a significant increase in BNP mRNA in the right and left atria from both male and female 8-week-old SHR. In the ventricles from both male and female SHR, there was no increase in the ratio of left ventricular wet weight/body weight, no increase in ventricular ANF mRNA transcripts, and no myosin heavy chain isoform switch (a protein marker of hypertrophy). irBNP ventricular concentration, however, increased significantly in both male and female SHR, but only in female SHR was there a concomitant increase in BNP mRNA. These results suggest that 1) ANF and BNP production are not coordinated in all cardiac compartments during the development of hypertension; 2) upregulation of BNP in the atria from male and female SHR is the earliest event detected at 8 weeks; 3) the prehypertensive stage, in the genetically hypertensive female rats, is associated with an increase in ventricular irBNP concentration and BNP mRNA; 4) there is a

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Alignment of Rat Cardionatrin Sequences with the Preprocardionatrin Sequence from Complementary DNA

Cited by 115 publications

References 27 publications

Variable Renal Atrial Natriuretic Factor Gene Expression in Hypertension

Variable Renal Atrial Natriuretic Factor Gene Expression in Hypertension

Effect of phorbol ester on the release of atrial natriuretic peptide from the hypertrophied rat myocardium

Atrial natriuretic factor and brain natriuretic peptide gene expression in the spontaneous hypertensive rat during postnatal development

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