C-type natriuretic peptide in individuals with normal left ventricular systolic function

Kuo, Jen‐Yuan; Yeh, Hung‐I; Chang, Sheng-Hsiung; Shih, Bing-Fu; Wang, An-Mei; Chen, Chun‐Yen; Hou, Charles Jia‐Yin

doi:10.1080/14017430701302482

Cited by 6 publications

(8 citation statements)

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“…In addition to supporting previous (and smaller) studies showing net cardiac release of CNP, 22,24,25 the present study relates these findings to cardiac function and reports new findings of CNP release by head and neck and lower limb tissues and extraction of CNP across hepatic, renal, and pulmonary tissues in adult humans.…”

Section: Discussionsupporting

confidence: 67%

“…Recent work, however, has shown that clinical states of cardiac impairment are associated with increases in circulating and coronary sinus CNP levels, 20 -22 which suggest that elevated cardiac tissue production of CNP may be associated with increasing myocardial dysfunction. Although individual studies have separately measured transcardiac [22][23][24][25] and transrenal 26 CNP immunoreactivity, little is known about CNP production and clearance across other organs in health or cardiovascular disease. Such studies have been hindered by the largely autocrine/paracrine nature of CNP with rapid local (and systemic) degradation through uptake by the clearance receptor 27 and hydrolysis by neprilysin and consequent very low circulating concentrations of CNP.…”

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confidence: 99%

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Regional Release and Clearance of C-Type Natriuretic Peptides in the Human Circulation and Relation to Cardiac Function

et al. 2009

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Abstract-Production and clearance of plasma C-type natriuretic peptide (CNP) and amino terminal (NT)-proCNP immunoreactivity in the human circulation remain poorly characterized. Accordingly, we have measured arterial and venous concentrations of CNP and NT-proCNP across multiple tissue beds during cardiac catheterization in 120 subjects (age: 64.2Ϯ9.0 years; 73% men) investigated for cardiovascular disorders. The heart, head and neck, and musculoskeletal tissues made the clearest contributions to both plasma CNP and NT-proCNP (PϽ0.05). Net release of NT-proCNP was also observed from hepatic tissue (PϽ0.001). Negative arteriovenous gradients for CNP were observed across renal, hepatic, and pulmonary tissue (PϽ0.05), indicating net clearance, whereas no tissue-specific site of NT-proCNP clearance was identified. Age, mean pulmonary artery pressure, left ventricular end diastolic pressure, Brandt score of myocardial jeopardy, and troponin I were independent predictors of circulating CNP levels in multivariable analysis. Sex and kidney function were independently predictive of arterial NT-proCNP. The proportional step-up of CNP (ϩ60%) across the heart was less than for brain natriuretic peptide (ϩ123%) but greater than for NT-pro-brain natriuretic peptide (NT-proBNP) (ϩ36%) and NT-proCNP (ϩ42%; PϽ0.001 for all). We conclude that cardiac and head and neck tissue are important sources of CNP. Circulating CNP but not NT-proCNP concentrations are related to cardiac hemodynamic load and ischemic burden. Although cardiac release is most evident, multiple additional tissues release NT-proCNP immunoreactivity without evidence for an organ-specific site for NT-proCNP degradation. Taken together, differences in magnitude and direction of transorgan gradients for CNP compared with NT-proCNP suggest net generalized cosecretion with differing mechanisms of clearance. Key Words: natriuretic peptides Ⅲ circulation Ⅲ plasma Ⅲ glomerular filtration rate Ⅲ human C -type natriuretic peptide (CNP), a vasoactive and antiproliferative peptide, 1,2 shares sequence homology and biological actions 3 with the endocrine cardiac peptides, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP). After the isolation of CNP from porcine brain tissue, 4 both CNP and CNP mRNA have been identified in vascular endothelium 5,6 and cardiac, 7,8 renal, 9 skeletal, 10 and reproductive 11,12 tissues. Although ANP and BNP activate the guanylate cyclase-coupled natriuretic peptide receptor (NPR)-A and promote natriuresis and diuresis, 3 CNP is the predominant ligand for another NPR, NPR-B, 13 which is also widely distributed in tissues including brain, 14 vascular endothelium, smooth muscle cells, 15 and myocardium. 16 Binding to NPR-B, CNP induces in vitro venodilatation, 17 cardiac inotropy, and chronotropy 18 and inhibits vascular smooth muscle proliferation. 15 Recent studies have shown that CNP exhibits antihypertrophic and antifibrotic properties during ventricular modeling after experimental myocardial infarction. 19 Distinct from ANP a...

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Section: Discussionsupporting

confidence: 67%

mentioning

confidence: 99%

Regional Release and Clearance of C-Type Natriuretic Peptides in the Human Circulation and Relation to Cardiac Function

et al. 2009

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“…Our laboratory previously found that the myocardium regularly produced or released CNP in patients with normal left ventricular (LV) systolic function. Brief periods of rapid right atrial (RA) pacing (with pacing cycle lengths starting from 750 ms, in 50-ms decrement, to a minimum of 400 ms, each for 2 min and rest for 2 min) or PSVT (sustained Ͻ2 min) did not change the production and/or release (13). The aim of this study was to compare the response of the three peptides against a 30-min induced PSVT.…”

mentioning

confidence: 99%

Responses of cardiac natriuretic peptides after paroxysmal supraventricular tachycardia: ANP surges faster than BNP and CNP

Kuo

Wang

Chang

et al. 2016

American Journal of Physiology-Heart and Circulatory Physiology

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Atrial natriuretic peptide (ANP) secretion increases after 30 min of paroxysmal supraventricular tachycardia (PSVT). Whether this phenomenon also applies to brain or C-type natriuretic peptides (BNP or CNP) remains unknown. Blood samples of 18 patients (41 ± 11 yr old; 4 men) with symptomatic PSVT and normal left ventricular systolic function (ejection fraction 65 ± 6%) were collected from the coronary sinus (CS) and the femoral artery (FA) before and 30 min after the induction, and 30 min after the termination of PSVT. The results showed that the ANP levels rose steeply after the PSVT and then reduced at 30 min after the termination (baseline vs. post-PSVT vs. posttermination: CS: 34.0 ± 29.6 vs. 74.1 ± 42.3 vs. 46.1 ± 32.9; FA: 5.9 ± 3.24 vs. 28.2 ± 20.7 vs. 10.0 ± 4.6 pg/ml; all P < 0.05). In contrast, compared with ANP, the increases of BNP and CNP in CS after the PSVT were less sharp, but continued to rise after the termination of tachycardia (BNP, 10.2 ± 6.4 vs. 11.3 ± 7.1 vs. 11.8 ± 7.9; CNP, 4.5 ± 1.2 vs. 4.9 ± 1.4 vs. 5.0 ± 1.4 pg/ml; all P < 0.05). The rise of BNP and CNP in FA was similarly less sharp after the PSVT and remained stationary after the termination. PSVT exerted differential effects on cardiac natriuretic peptide levels. ANP increased greater after a 30-min induced PSVT, but dropped faster after termination of PSVT, compared with BNP and CNP.

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“…Kuo et al28) reported that the myocardium regularly produces or releases CNP in patients with symptomatic paroxysmal supraventricular tachycardia (PSVT) and normal left ventricular systolic function and brief periods of rapid atrial pacing, and that PSVT or electrophysiological studies did not change the production and/or release of CNP. Lupattelli et al29) suggested that CNP was not altered in patients affected by hypercholesterolemia.…”

Section: Discussionmentioning

confidence: 99%

C-Type Natriuretic Peptide as a Surrogate Marker in Variant Angina Pectoris

et al. 2013

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Background and ObjectivesThe purpose of this study was to assess the value of C-type natriuretic peptide (CNP) as a surrogate marker for detection of coronary artery spasm in variant angina pectoris (VAP).Subjects and MethodsSixty-six patients (mean age: 51±11 years, M : F=40 : 26) who underwent coronary angiography on suspicion of angina and who were diagnosed with VAP by the acetylcholine-induced spasm provocation test (SPT) were enrolled and divided into a SPT (-) group (n=23) and a SPT (+) group (n=43). Concentrations of CNP and other markers were determined by immunoassay in both groups.ResultsPlasma CNP and creatine kinase myoglobin band (CK-MB) concentrations were significantly increased in the SPT (+) group relative to the SPT (-) group (CNP, 5.268±1.800 pg/mL vs. 3.342±1.150 pg/mL, p=0.002; CK-MB, 2.54±1.03 ng/dL vs. 1.86±0.96 ng/dL, p=0.019, respectively) while plasma high sensitivity C-reactive protein (hs-CRP) and N-terminal pro-brain natriuretic peptide (NT pro-BNP) concentrations were not significantly different between the SPT (-) group and SPT (+) group (hs-CRP, 2.76±4.99 mg/L vs. 3.13±4.88 mg/L, p=0.789; NT pro-BNP, 49±47 pg/mL vs. 57±63 pg/mL, p=0.818, respectively). Plasma CNP concentration was independently associated with the VAP via SPT {odds ratio: 2.014 (95% confidence interval: 1.016-3.992), p=0.045}. A CNP cut-off value of 4.096 pg/mL was found to have a sensitivity of 68.2% and a specificity of 40.0% for predicting the probability of VAP via SPT.ConclusionIncreased plasma CNP concentration in patients with VAP may have an impact on the regulation of endothelial function in accordance with the progression of atherosclerosis. Further analysis is warranted to develop clinical applications of this finding.

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C-type natriuretic peptide in individuals with normal left ventricular systolic function

Abstract: The myocardium regularly produces or releases CNP in patients with normal LV systolic function. Brief periods of rapid RA pacing, PSVT, or EPS does not change the production and/or release.

Cited by 6 publications

References 20 publications

Regional Release and Clearance of C-Type Natriuretic Peptides in the Human Circulation and Relation to Cardiac Function

Regional Release and Clearance of C-Type Natriuretic Peptides in the Human Circulation and Relation to Cardiac Function

Responses of cardiac natriuretic peptides after paroxysmal supraventricular tachycardia: ANP surges faster than BNP and CNP

C-Type Natriuretic Peptide as a Surrogate Marker in Variant Angina Pectoris

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