The Heart and the Atrial Natriuretic Factor*

Cantin, M.; Genest, Jacques

doi:10.1210/edrv-6-2-107

Cited by 749 publications

(175 citation statements)

References 143 publications

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“…Atrial natriuretic peptide (ANP), a peptide hormone that regulates salt and water balance and blood pressure, is synthesized, stored, and secreted from mammalian myocytes (Cantin & Genest, 1985;Lang et al, 1985;Brenner & Ballerman, 1986;Ruskoaho et al, 1987;Needleman et al, 1989). The major site of ANP biosynthesis is the atria of the heart, where it constitutes 1-3% of the total messenger RNA (mRNA) (Needleman et al, 1989).…”

Section: Introductionmentioning

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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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: Introductionmentioning

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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“…It is generally recognized as a multifactorial disease associated with etiological factors, and both genetic and environmental factors have been implicated sure and volume homeostasis [5,8]. This peptide hormone is mainly produced in the cardiac atria, where it is stored within secretory granules as a large precursor (proANP), which is the major component of the granules [5,7,27].…”

Section: Introductionmentioning

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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“…Atrial cardiocytes in most vertebrates and also ventricular cardiocytes in non mammalian ones are able to produce a family of atrial natriuretic peptides (ANP) (Cantin & Genest, 1985;Chapeau et al, 1985;Netchitailo et al, 1988;Reinecke et al, 1988;Gilles et al, 1990;Takei, 2000). The prohormone of this family is a 126 amino acid precursor which is stored in granules and generates, as a biologically active form, a 28 amino acid C-terminal fragment which exerts a variety of biological effects including diuresis, natriuresis and vasorelaxing effects through the action of specific membrane receptors linked to the enzyme guanylate cyclase (GC) (Forssmann et al, 1998).…”

Section: Introductionmentioning

confidence: 99%