Natriuretic peptide C receptor signalling in the heart and vasculature

Rose, Robert A.; Giles, Wayne R.

doi:10.1113/jphysiol.2007.144253

Cited by 186 publications

(157 citation statements)

References 115 publications

(213 reference statements)

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“…6R) and cells without typical transients ($70%, Fig. 6S signaling in a number of cell types via cGMP/Gi or Gi/NOS pathways, respectively (Ji et al, 1999;Rose and Giles, 2008; Fig. 7A).…”

Section: Mlc2vmentioning

confidence: 99%

Functional characterization of cardiac progenitor cells and their derivatives in the embryonic heart post‐chamber formation

McMullen

Zhang

Hotchkiss

et al. 2009

Developmental Dynamics

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There is scant information on the fate of cardiac progenitor cells (CPC) in the embryonic heart after chamber specification. Here we simultaneously tracked three lineage-specific markers (Nkx2.5, MLC2v, and ANF) and confirmed that CPCs with an Nkx2.5 1 MLC2v 2 ANF 2 phenotype are present in the embryonic (E) day 11.5 mouse ventricular myocardium. We demonstrated that these CPCs could give rise to working cardiomyocytes and conduction system cells. Using a two-photon imaging analysis, we found that the majority of CPCs are not capable of developing Ca 21 transients in response to b-adrenergic receptor stimulation. In contrast, Nkx2.5 1 cells expressing MLC2v but not ANF are capable of developing functional Ca 21 transients. We showed that Ca 21 transients could be invoked in Nkx2.5 1 MLC2v 1 ANF 1 cells only upon inhibition of Gi, muscarinic receptors, or nitric oxide synthase (NOS) signaling pathways. Our data suggest that these inhibitory pathways may delay functional specification in a subset of developing ventricular cells.

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“…6R) and cells without typical transients ($70%, Fig. 6S signaling in a number of cell types via cGMP/Gi or Gi/NOS pathways, respectively (Ji et al, 1999;Rose and Giles, 2008; Fig. 7A).…”

Section: Mlc2vmentioning

confidence: 99%

Functional characterization of cardiac progenitor cells and their derivatives in the embryonic heart post‐chamber formation

McMullen

Zhang

Hotchkiss

et al. 2009

Developmental Dynamics

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“…Atrial natriuretic peptide (ANP), B-type natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) are members of the natriuretic peptide family of bioactive peptides best known for their role in the regulation of blood pressure and cardiovascular homeostasis [1,2]. The cellular responsiveness of natriuretic peptides is manifested through the specific cell surface receptors in different target tissues [1].…”

Section: Introductionmentioning

confidence: 99%

Relaxant effect of brain natriuretic peptide in nonsensitized and passively sensitized isolated human bronchi

Matera

Calzetta

Parascandolo

et al. 2009

Pulmonary Pharmacology & Therapeutics

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. M A N U S C R I P T A C C E P T E D ARTICLE IN PRESS

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“…The natriuretic peptide clearance receptor (NPR-C) lacks guanylyl cyclase activity and functions primarily to clear natriuretic peptides from the circulation. However, a signaling function has been proposed for this receptor as well (2).…”

mentioning

confidence: 99%

Novel Bifunctional Natriuretic Peptides as Potential Therapeutics

Dickey

Burnett

Potter

2008

Journal of Biological Chemistry

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Synthetic atrial natriuretic peptide (carperitide) and B-type natriuretic peptide (BNP; nesiritide) are used to treat congestive heart failure. However, despite beneficial cardiac unloading properties, reductions in renal perfusion pressures limit their clinical effectiveness. Recently, CD-NP, a chimeric peptide composed of C-type natriuretic peptide (CNP) fused to the C-terminal tail of Dendroaspis natriuretic peptide (DNP), was shown to be more glomerular filtration rate-enhancing than BNP in dogs. However, the molecular basis for the increased responsiveness was not determined. Here, we show that the DNP tail has a striking effect on CNP, converting it from a nonagonist to a partial agonist of natriuretic peptide receptor (NPR)-A while maintaining the ability to activate NPR-B. This effect is specific for human receptors because CD-NP was only a slightly better activator of rat NPR-A due to the promiscuous nature of CNP in this species. Interesting, the DNP tail alone had no effect on any NPR even though it is effective in vivo. To further increase the potency of CD-NP for NPR-A, we converted two different triplet sequences within the CNP ring to their corresponding residues in BNP. Both variants demonstrated increased affinity and full agonist activity for NPR-A, whereas one was as potent as any NPR-A activator known. In contrast to a previous report, we found that DNP binds the natriuretic peptide clearance receptor (NPR-C). However, none of the chimeric peptides bound NPR-C with significantly higher affinity than endogenous ligands. We suggest that bifunctional chimeric peptides represent a new generation of natriuretic peptide therapeutics.The human natriuretic peptide system consists of atrial natriuretic peptide (ANP), 2 B-type natriuretic peptide (BNP), C-type natriuretic peptide (CNP), and an N-terminally extended renal form of ANP called urodilatin (1). ANP, BNP, and urodilatin bind natriuretic peptide receptor (NPR)-A, whereas CNP binds NPR-B. Both receptors are transmembrane guanylyl cyclases, which when activated catalyze the synthesis of cGMP. The natriuretic peptide clearance receptor (NPR-C) lacks guanylyl cyclase activity and functions primarily to clear natriuretic peptides from the circulation. However, a signaling function has been proposed for this receptor as well (2).Both ANP and BNP reduce blood pressure by increasing natriuresis, diuresis, vasodilation, and endothelial permeability. They also prevent cardiac hypertrophy and suppress the reninangiotensin-aldosterone systems. In 2001, BNP was approved by the United States Food and Drug Administration for the treatment of acutely decompensated heart failure. However, recent reports have suggested impaired renal function, which may be related to excessive hypotension (3, 4).CD-NP represents a new class of natriuretic peptide drug that may circumvent the hypotensive nature of BNP and preserve or augment renal function in the congestive heart failure setting. CD-NP contains the full-length 22-amino acid human CNP fused to the 15-amino acid C...

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Natriuretic peptide C receptor signalling in the heart and vasculature

Cited by 186 publications

References 115 publications

Functional characterization of cardiac progenitor cells and their derivatives in the embryonic heart post‐chamber formation

Functional characterization of cardiac progenitor cells and their derivatives in the embryonic heart post‐chamber formation

Relaxant effect of brain natriuretic peptide in nonsensitized and passively sensitized isolated human bronchi

Novel Bifunctional Natriuretic Peptides as Potential Therapeutics

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