Expression and distribution of atrial natriuretic peptide in human hypertrophic ventricle of hypertensive hearts and hearts with hypertrophic cardiomyopathy.

Takemura, Genzou; Fujiwara, Hisayoshi; Mukoyama, Masashi; Saito, Yoshihiko; Nakao, Kazuwa; Kawamura, Atsushi; Ishida, Moriharu; Kida, Mitsugu; Uegaito, Takashi; Tanaka, Masaru

doi:10.1161/01.cir.83.1.181

Cited by 61 publications

(34 citation statements)

References 44 publications

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“…Upregulation of ANF gene expression is a highly conserved genetic marker of ventricular hypertrophy both in vitro and in vivo. It occurs in response to a wide variety of hypertrophic stimuli and across highly divergent species (3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14). Since the pattern of cardiac gene expression associated with ventricular hypertrophy is very similar to that observed in the embryonic heart, it has been hypothesized that similar mechanisms may mediate induction of the embryonic genes in both situations.…”

Section: Introductionmentioning

confidence: 99%

Divergent pathways mediate the induction of ANF transgenes in neonatal and hypertrophic ventricular myocardium.

Knowlton

Rockman²,

Itani³

et al. 1995

J. Clin. Invest.

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To determine whether similar or divergent pathways mediate atrial natriuretic factor (ANF) induction in neonatal and hypertrophied adult ventricular myocardium, and to assess whether studies using an in vitro model system of hypertrophy have fidelity to the in vivo context during pressure overload hypertrophy, we generated transgenic mice which harbor either 638 or 3,003 bp of the rat ANF 5' flanking region ligated upstream from a luciferase reporter. Luciferase activity in the ventricles of day 1 transgenic neonates was 8-24-fold higher than the levels expressed in the ventricles of adult mice. Adult mice expressed the luciferase reporter in an appropriate tissue-specific manner. Transverse aortic constriction of adult mice harboring ANF reporter transgenes demonstrated no significant increase in reporter activity in the ventricle. These findings demonstrate that distinct regions of the ANF 5'-flanking region are required for inducible expression of the ANF gene in the hypertrophic adult ventricle compared with those required for atrial-specific and developmentally appropriate expression in the intact neonatal heart. Furthermore, the cis regulatory elements necessary for induction of ANF expression in endothelin-1 or a1-adrenergically stimulated cultured neonatal ventricular myocytes are not sufficient for induction in the in vivo context of pressure overload hypertrophy. (J. Clin.

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Section: Introductionmentioning

confidence: 99%

Divergent pathways mediate the induction of ANF transgenes in neonatal and hypertrophic ventricular myocardium.

Knowlton

Rockman²,

Itani³

et al. 1995

J. Clin. Invest.

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“…Takemura et al showed that, in a selected population of HCM patients, the ventricular ANP gene expresses in response to disease-specific changes (eg, myocardial fiber disarray, hypertrophy of myocytes and fibrosis) rather than as an adaptative response. 33 There might be unknown causes of the high plasma concentrations of ANP and BNP in some HCM patients and further studies are needed.…”

Section: Discussionmentioning

confidence: 98%

“…Additionally, ANP mRNA has been detected in the ventricles of patients with HCM. 33 Thus, the high plasma concentrations of ANP detected in HCM patients may have originated mainly from the left ventricle.…”

Section: Discussionmentioning

confidence: 99%

Neurohumoral Profiles in Patients With Hypertrophic Cardiomyopathy-Differences to Hypertensive Left Ventricular Hypertrophy-

Oginö¹,

Ogura²,

Kuboi

et al. 2004

Circ J

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ypertrophic cardiomyopathy (HCM) characteristically has severe myocardial hypertrophy, predominantly involving the interventricular septum of the nondilated left ventricle. Echocardiography is useful for the differential diagnosis of HCM, but it can be difficult to distinguish HCM from hypertensive heart disease (HHD) with left ventricular (LV) hypertrophy. Although concentric LV hypertrophy is observed in patients with HCM 1 and sometimes HCM patients present with hypertension as a complication, asymmetrical interventricular hypertrophy (ASH) is also observed in HHD. 2,3 Recently, ultrasonic myocardial tissue characterization by integrated backscatter has provided additional information about the pathological changes; however, it is still unable to completely differentiate HCM from HHD. 4 It has been reported that various neurohumoral systems are accelerated in patients with HHD or HCM. In HHD, the plasma concentrations of epinephrine and norepinephrine are increased, 5,6 and other trophic neurohumoral factors, such as angiotensin II 7 and endothelin-1, 8 are also increased. Moreover, it has been reported that atrial natriuretic peptide (ANP) is increased in patients with hypertension. 9 With regard to HCM patients, it has been reported that plasma concentrations of catecholamines 10 and endothelin-1 11 are increased, as well as those of ANP and brain natriuretic peptide (BNP). [12][13][14][15][16] However, there are no data on the differences in the neurohumoral profiles of HCM and HHD patients.Thus, in the present study we measured the plasma concentrations of catecholamines (epinephrine and norepinephrine), angiotensin II, endothelin-1 and natriuretic peptides (ANP and BNP) in patients with HCM and HHD without LV dysfunction to clarify the neurohumoral profile of HCM and its clinical implications. Methods SubjectsWe studied 40 patients with HCM, 35 with HHD and 15 healthy normal controls (Protocol 1). All patients were clinically evaluated and carefully diagnosed based on their family history, history of hypertension, echocardiography (UCG) and cardiac catheterization. 17,18 Patients with angina pectoris, low LV ejection fraction (LVEF: <50%), valvular heart disease, liver injury or renal dysfunction were excluded because all of these factors have effects on the Circ J 2004; 68: 444 -450 (Received November 28, 2003; revised manuscript received February 6, 2004; accepted February 13, 2004 Background Patients with hypertrophic cardiomyopathy (HCM) or hypertensive heart disease (HHD) have increased concentrations of various neurohumoral factors. Thus, the aim of the present study was to evaluate the differences in the neurohumoral profiles of HCM and HHD. Methods and Results Plasma concentrations of epinephrine, norepinephrine, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), angiotensin II and endothelin-1 were measured in 40 patients with HCM, 35 with HHD, and 15 controls. Additionally, the concentrations of these neurohumoral factors in the coronary sinus and aortic root were measured in...

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“…In support of this we note that the ventricular ANP mRNA level in THM was approximately 40-fold higher than that in normotensive mice, and corresponded with an increase in ventricular ANP concentration. ANP is also synthesized in the working myocytes in the ventricle of a hypertensive heart [2,31], a heart with hypertrophic cardiomyopathy [33,38] and in heart failure [43] as the urgent circulating hormone. The manner of the secretion of ANP in the diseased heart may be associated with some augmented biosynthesis of ANP in the ventricular cardiocytes.…”

Section: Discussionmentioning

confidence: 99%

A-type Natriuretic Peptide Level in Hypertensive Transgenic Mice

et al. 2004

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A-type (atrial) natriuretic peptide (ANP) levels in heart and plasma were examined by immunohistochemistry, electron microscopy, and radioimmunoassay (RIA) in hypertensive transgenic mice (Tsukuba hypertensive mice; THM). Additionally, the ANP mRNA level in the heart was measured using real-time polymerase chain reaction (PCR) assay. The blood pressure and the ratio of heart weight to body weight in THM was significantly higher than those in the control mice (C57BL/6J). The number of ANPgranules and ANP immunoreactivity in the auricular cardiocytes were significantly lower in THM than in the control. Ultrastructurally, the ventricular cardiocytes in the THM occasionally had ANP-like granules, which were not present in the controls. Using RIA, the plasma, auricular, and ventricular ANP concentrations were significantly higher in THM than in the control, but there was no significant difference in plasma cyclic guanosine monophosphate (GMP) concentration between THM and the control. The ANP mRNA levels of the auricular and ventricular cardiocytes in the THM were siginificantly higher than those in the controls. The present study suggested that the ANP release system of the auricular cardiocytes in these transgenic mice is different from normal (control mice). Key words: A-type natriuretic peptide, hypertension, transgenic mice, cardiocyte in its etiology [21]. Several complex physiological systems affect blood pressure, including one that is mediated by the 28-amino acid A-type (atrial) natriuretic peptide (ANP) [13,21]. ANP is a circulating hormone with a wide range of biological effects, including natriuresis, diuresis and vasodilation, and it plays an important role in the regulation of blood pres-

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Expression and distribution of atrial natriuretic peptide in human hypertrophic ventricle of hypertensive hearts and hearts with hypertrophic cardiomyopathy.

Cited by 61 publications

References 44 publications

Divergent pathways mediate the induction of ANF transgenes in neonatal and hypertrophic ventricular myocardium.

Divergent pathways mediate the induction of ANF transgenes in neonatal and hypertrophic ventricular myocardium.

Neurohumoral Profiles in Patients With Hypertrophic Cardiomyopathy-Differences to Hypertensive Left Ventricular Hypertrophy-

A-type Natriuretic Peptide Level in Hypertensive Transgenic Mice

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