Diverse biological actions of atrial natriuretic peptide

Brenner, Barry M.; Ballermann, Barbara J.; Gunning, M.; Zeidel, Mark L.

doi:10.1152/physrev.1990.70.3.665

Cited by 855 publications

(532 citation statements)

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“…CNP is somewhat selectively predominant in the central nervous system [5,6], hence it is possible that it acts as a neurotransmitter and/or participates in the centrally-related fluid secretion and blood pressure regulation. One important second messenger of these hormones is cyclic GMP (reviewed in [2][3][4]). The receptors for ANF (ANF-RGC) [7-l 31 and CNP (CNP-RGC) [ 14,151 have been characterized; both are guanylate cyclases and are structurally similar.…”

Section: Introductionmentioning

confidence: 99%

The glycine residue of ATP regulatory module in receptor guanylate cyclases that is essential in natriuretic factor signaling

1993

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Atrial natriuretic factor (ANF) and C-type natriuretic peptide (CNP)-activated guanylate cyclases are single-chain transmembrane-spanning proteins, containing both ligand binding and catalytic activities. In both proteins, ligand binding to the extracellular receptor domain activates the cytosolic catalytic domain, generating the second messenger cyclic GMP. Obligatory in this activation process is an ATP-dependent step. ATP directly binds to a deBned ATP-regulatory module (ARM) sequence motif in the cyclases and through ARM bridges the events of ligand binding and signal transduction. These ARM sequence motifs are respectively represented by GlySo'-Xa-Gl$05-Xa-Xa-Xa-Gly509 and Gly@-Xa-Xa-XaGly"' in the case of ANF receptor guanylate cyclase (ANF-RGC) and CNP receptor guanylate cyclase (CNP-RGC). Through genetic remodeling techniques, we now show that ARM-GlJo5 in ANF-RGC and the corresponding ARM-Gly"% in CNP-RGC are critical for ANF and CNP signaling, and other ARM-Gly residues have minimal effect in the respective signaling processes.Guanylate cyclase; ATP-regulatory module; Atrial natriuretic factor receptor; Type C natriuretic peptide receptor

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Section: Introductionmentioning

confidence: 99%

The glycine residue of ATP regulatory module in receptor guanylate cyclases that is essential in natriuretic factor signaling

1993

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“…The natriuretic peptides comprise a family of vasoactive hormones that play an important role in the regulation of cardiovascular and renal homeostasis (1). Their natriuretic and vasodepressor properties suggest that they represent endogenous antagonists of the various systems (e.g.…”

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confidence: 99%

Mechanical Strain Increases Expression of the Brain Natriuretic Peptide Gene in Rat Cardiac Myocytes

Liang

Garami³

et al. 1997

Journal of Biological Chemistry

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Using a device that applies cyclical strain (1 Hz) to ventricular cardiocytes cultured on collagen-coated silicone elastomer surfaces, we have demonstrated straindependent increases in brain natriuretic peptide (BNP) secretion, BNP mRNA levels, and expression of a transiently transfected ؊1595 human BNP-luciferase reporter. When actinomycin D (10 M) was introduced concomitantly with the strain stimulus, the strain-induced increase in BNP mRNA was eliminated, and the decay of transcripts was identical in the control and strained cells, indicating the lack of independent effects on transcript stability. Strain-dependent ؊1595 human BNPluciferase activity was completely inhibited by chelerythrine, 2-aminopurine, genistein, and W-7 and only partially or not at all by KN-62, wortmannin, and H-89. The effects of these individual agents paralleled their effects on mitogen-activated protein kinase (MAPK) activity, but not c-Jun N-terminal kinase (JNK) activity, in the cells. Overexpression of wild-type MAPK and, to a lesser extent, JNK increased strain-dependent BNP promoter activity, whereas dominant-negative mutants of MAPK kinase, JNK kinase, or Ras completely blocked strain-dependent reporter activity. These findings provide the first demonstration that mechanical strain can increase myocardial gene expression through a transcriptional mechanism and suggest important roles for MAPK and JNK in mediating this effect.The natriuretic peptides comprise a family of vasoactive hormones that play an important role in the regulation of cardiovascular and renal homeostasis (1). Their natriuretic and vasodepressor properties suggest that they represent endogenous antagonists of the various systems (e.g. renin-angiotensin system and sympathetic nervous system) that support arterial blood pressure under basal conditions and, at times, contribute to the pathophysiology of cardiovascular disease.Atrial natriuretic peptide (ANP), 1 the prototype of the group, is produced primarily in the atria of the heart. ANP is expressed in the cardiac ventricle during development and early neonatal life (2, 3). Expression decays as the animal ages and remains quiescent in the adult unless the ventricle is subjected to hemodynamic overload (i.e. mechanical strain that leads to increased wall stress and subsequently to hypertrophy of the myocardium), as occurs with systemic arterial hypertension or congestive heart failure (4 -7).Brain natriuretic peptide (BNP) is also produced in the heart. Despite the nomenclature, relatively little BNP is expressed in the mammalian brain (the exception being the porcine brain, where the peptide was identified originally). Expression of BNP in the heart is lower than that of ANP under basal conditions, and the atrial/ventricular ratio of expression is considerably less than that seen with ANP (8). Ventricular expression of BNP is activated in a fashion similar to ANP in pathophysiological states associated with hemodynamic overload (9, 10). At some stages of advanced congestive heart failure, circulating BNP le...

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“…In our preliminary experiment, systemic administration of dog BNP (20-200 p mol/kg, iv) reduced cardiac output and aortic pressure dose-dependently, but eel VNP did not decrease cardiac output significantly in the dog (Arai M, Goto F: unpublished data). In the eel and rat, tachyphylaxis was induced by eel VNP (1-36) for vasodepressor effects in both species, but it was not observed in C-terminally truncated eel VNP (1-25) and mammalian ANP, BNP or CNP [5,11]. These data suggest the unique cardiovascular effect of eel VNP compared with BNP may derive from its C-terminal sequence.…”

Section: Discussionmentioning

confidence: 88%

Effect of Eel Ventricular Natriuretic Peptide on the Kidney and Cardiovascular System in the Dog.

1996

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Abstract.Ventricular natriuretic peptide (VNP), a possibly new type of natriuretic peptide with an extended C-terminal tail, has been isolated from eel cardiac ventricles. We investigated the effects of eel VNP on the kidney and cardiovascular system and compared these results with those of mammalian peptides in dogs. Eel VNP, human (dog) ANP, human and dog BNPs were infused into the renal artery at non-hypotensive doses.All peptides produced similar diuresis and natriuresis, but cardiac output and the left and right ventricular stroke work were decreased by BNPs, but ANP and eel VNP did not change these parameters.Systemic vascular resistance was increased by BNPs, but unaffected by other peptides. These results show that eel VNP has renal effects similar to ANP and BNP, but it elicits responses in the heart different from those of BNPs in anesthetized dogs.

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Diverse biological actions of atrial natriuretic peptide

Cited by 855 publications

References 0 publications

The glycine residue of ATP regulatory module in receptor guanylate cyclases that is essential in natriuretic factor signaling

The glycine residue of ATP regulatory module in receptor guanylate cyclases that is essential in natriuretic factor signaling

Mechanical Strain Increases Expression of the Brain Natriuretic Peptide Gene in Rat Cardiac Myocytes

Effect of Eel Ventricular Natriuretic Peptide on the Kidney and Cardiovascular System in the Dog.

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