Natriuretic Peptides

Epstein, Franklin H.; Levin, Ellis R.; Gardner, David G.; Samson, Willis K.

doi:10.1056/nejm199807303390507

Cited by 1,870 publications

(402 citation statements)

References 54 publications

Supporting

Mentioning

391

Contrasting

Unclassified

Order By: Relevance

“…Physiologically, BNP leads to vasodilatation through inhibition of the renin and aldosterone production, inhibition of the sympathetic nervous system activity, and induction of diuresis. 22,23 Beside these indirect effects on the vessels, BNP may exert its effect also directly. In vitro studies have demonstrated that BNP activates the guanylate cyclase receptors, on both endothelial and vascular smooth muscle cells, which subsequently activate potassium and calcium channels promoting arterial vasodilatation.…”

Section: Discussionmentioning

confidence: 99%

N-Terminal Pro-B–Type Natriuretic Peptide Is Related to Retinal Microvascular Damage

Mutlu

Ikram

Hofman

et al. 2016

ATVB

View full text Add to dashboard Cite

Objective— N-terminal pro-B–type natriuretic peptide (NT-proBNP) is a marker of cardiac dysfunction and has been linked to various indices of large vessel disease. However, it remains unclear whether NT-proBNP also relates to microvascular damage. In a community-dwelling population, we studied the association between NT-proBNP and retinal microvascular damage. Approach and Results— From the population-based Rotterdam Study, we included 8437 participants (mean age 64.1 years and 59% women) without a history of cardiovascular disease, with NT-proBNP data and gradable retinal images. NT-proBNP serum levels were measured using an immunoassay. Retinopathy signs, that is, exudates, microaneurysms, cotton wool spots, and dot/blot hemorrhages, present on fundus photographs were graded in the total study population; retinal vascular calibers, that is, arteriolar and venular calibers, were semiautomatically measured in a subsample (n=2763) of the study population. We conducted cross-sectional analyses on the association between NT-proBNP and retinal microvascular damage using logistic and linear regression models, adjusting for age, sex, and cardiovascular risk factors. We found that NT-proBNP was associated with the presence of retinopathy (adjusted odds ratio [95% confidence interval] per SD increase in natural log-transformed NT-proBNP: 1.14 [1.03–1.27]). We also found that higher NT-proBNP was associated with narrower arteriolar calibers (adjusted mean difference in arteriolar caliber per SD increase in natural log-transformed NT-proBNP: −0.89 µm [−1.54 to −0.24]). This association remained unchanged after excluding participants with retinopathy signs. Conclusions— In participants free of clinical cardiovascular disease, higher levels of NT-proBNP are associated with retinal microvascular damage, suggesting a potential role for NT-proBNP as marker for small vessel disease.

show abstract

Section: Discussionmentioning

confidence: 99%

N-Terminal Pro-B–Type Natriuretic Peptide Is Related to Retinal Microvascular Damage

Mutlu

Ikram

Hofman

et al. 2016

ATVB

View full text Add to dashboard Cite

show abstract

“…79 Hodgson-Zingman et al 80 described a family with AF and an autosomal dominant pattern of inheritance. In this family, a heterozygous frameshift mutation in NPPA was detected and the mutation co-segregated with AF.…”

Section: Non-ion Channel Mutationsmentioning

confidence: 99%

Atrial fibrillation: the role of common and rare genetic variants

Olesen

Nielsen

Haunsø³

et al. 2013

Eur J Hum Genet

105

View full text Add to dashboard Cite

Atrial fibrillation (AF) is the most common cardiac arrhythmia affecting 1-2% of the general population. A number of studies have demonstrated that AF, and in particular lone AF, has a substantial genetic component. Monogenic mutations in lone and familial AF, although rare, have been recognized for many years. Presently, mutations in 25 genes have been associated with AF. However, the complexity of monogenic AF is illustrated by the recent finding that both gain-and loss-of-function mutations in the same gene can cause AF. Genome-wide association studies (GWAS) have indicated that common single-nucleotide polymorphisms (SNPs) have a role in the development of AF. Following the first GWAS discovering the association between PITX2 and AF, several new GWAS reports have identified SNPs associated with susceptibility of AF. To date, nine SNPs have been associated with AF. The exact biological pathways involving these SNPs and the development of AF are now starting to be elucidated. Since the first GWAS, the number of papers concerning the genetic basis of AF has increased drastically and the majority of these papers are for the first time included in a review. In this review, we discuss the genetic basis of AF and the role of both common and rare genetic variants in the susceptibility of developing AF. Furthermore, all rare variants reported to be associated with AF were systematically searched for in the Exome Sequencing Project Exome Variant Server.

show abstract

“…10,12 ANP is produced in atrial myocytes and is released into the circulation in response to atrial stretch. ANP is best known for its ability to regulate blood volume and blood pressure through effects in the kidneys (natriuresis and diuresis) and blood vessels (smooth muscle relaxation and endothelial permeability).…”

mentioning

confidence: 99%

Effects of Wild-Type and Mutant Forms of Atrial Natriuretic Peptide on Atrial Electrophysiology and Arrhythmogenesis

Hua

MacLeod

Polina

et al. 2015

Circ: Arrhythmia and Electrophysiology

View full text Add to dashboard Cite

Background-Atrial natriuretic peptide (ANP) is a hormone with numerous beneficial cardiovascular effects. Recently, a mutation in the ANP gene, which results in the generation of a mutant form of ANP (mANP), was identified and shown to cause atrial fibrillation in people. The mechanism(s) through which mANP causes atrial fibrillation is unknown. Our objective was to compare the effects of wild-type ANP and mANP on atrial electrophysiology in mice and humans. Methods and Results-Action potentials (APs), L-type Ca 2+ currents (I Ca,L ), and Na + current were recorded in atrial myocytes from wild-type or natriuretic peptide receptor C knockout (NPR-C −/− ) mice. In mice, ANP and mANP (10-100 nmol/L) had opposing effects on atrial myocyte AP morphology and I Ca,L . ANP increased AP upstroke velocity (V max ), AP duration, and I Ca,L similarly in wild-type and NPR-C −/− myocytes. In contrast, mANP decreased V max , AP duration, and I Ca,L , and these effects were completely absent in NPR-C −/− myocytes. ANP and mANP also had opposing effects on I Ca,L in human atrial myocytes. In contrast, neither ANP nor mANP had any effect on Na + current in mouse atrial myocytes. Optical mapping studies in mice demonstrate that ANP sped electric conduction in the atria, whereas mANP did the opposite and slowed atrial conduction. Atrial pacing in the presence of mANP induced arrhythmias in 62.5% of hearts, whereas treatment with ANP completely prevented the occurrence of arrhythmias. Conclusions-These findings provide mechanistic insight into how mANP causes atrial fibrillation and demonstrate that wildtype ANP is antiarrhythmic.

show abstract

Natriuretic Peptides

Cited by 1,870 publications

References 54 publications

N-Terminal Pro-B–Type Natriuretic Peptide Is Related to Retinal Microvascular Damage

N-Terminal Pro-B–Type Natriuretic Peptide Is Related to Retinal Microvascular Damage

Atrial fibrillation: the role of common and rare genetic variants

Effects of Wild-Type and Mutant Forms of Atrial Natriuretic Peptide on Atrial Electrophysiology and Arrhythmogenesis

Contact Info

Product

Resources

About