Differential regulation of natriuretic peptide receptor messenger RNAs during the development of cardiac hypertrophy in the rat.

Brown, Lesley A.; Nunez, Derek J.; Wilkins, Martin R.

doi:10.1172/jci116887

Cited by 74 publications

(43 citation statements)

References 86 publications

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“…1 Of note, in the adult rat ventricle, the CNP receptor (NPR-B) has been identified predominantly in nonmyocyte cells. 16 Augmented expression of NPR-B occurs during development of cardiac hypertrophy after experimen- tal volume overload, 39 findings that suggest that CNP activity is increased in response to increasing myocardial wall tension. Because CNP potently suppresses both cardiac DNA and collagen synthesis in cardiac fibroblasts, these findings collectively suggest an important cardioprotective role for CNP in modulating cardiac fibrosis and extracellular matrix formation, in contrast to the natriuretic role for ANP and BNP in response to increasing cardiac-filling pressures.…”

Section: Discussionmentioning

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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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: Discussionmentioning

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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“…Myocardial cyclic GMP levels have been reported to be elevated in other types of heart failure and hypertrophy (17)(18)(19). There have been reported changes in atrial natriuretic peptide receptors that affect cyclic GMP in cardiac hypertrophy (36). In addition, muscarinic receptors are affected by pressure load-induced hypertrophy in the dog (37).…”

Section: Discussionmentioning

confidence: 99%

Increased guanylate cyclase activity is associated with an increase in cyclic guanosine 3',5'-monophosphate in left ventricular hypertrophy.

Sadoff¹,

Scholz²,

Tse³

et al. 1996

J. Clin. Invest.

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Left ventricular hypertrophy (LVH) produced by aortic valve plication leads to increased myocardial cyclic GMP. We tested whether this was a result of increased soluble guanylate cyclase activity or nitric oxide (NO) synthase and its functional consequences. We used the nitric oxide donor 3-morpholino-sydnonimine (SIN-1) or the NO synthase inhibitor N G -nitro-l-arginine methyl ester (L-NAME) in 12 control and 12 LVH anesthetized open-chest mongrel dogs. L-NAME (6 mg/kg) or SIN-1 (1 g/kg per min) was infused into the left anterior descending coronary artery and regional segment work and cyclic GMP levels were determined. In vitro myocardial guanylate cyclase sensitivity (0.43 Ϯ 0.04 to 0.28 Ϯ 0.04 mM [EC 50 ]) and maximal activity (10.1 Ϯ 2.9 to 25.5 Ϯ 6.5 pmol/mg protein per min) were significantly increased in LVH as compared with control animals in response to nitroprusside stimulation, but cyclic GMP-phosphodiesterase activity was similar. In LVH dogs, basal cyclic GMP was significantly elevated in vivo when compared with controls. Treatment of dogs with SIN-1 resulted in a significant increase in cyclic GMP in control (1.09 Ϯ 0.12 to 1.48 Ϯ 0.19 pmol/gram) and a greater increase in the LVH group (1.78 Ϯ 0.16 to 3.58 Ϯ 0.71 pmol/g). L-NAME had no effect on myocardial cyclic GMP levels in control or LVH dogs. Segment work decreased in the control group after SIN-1 (1,573 Ϯ 290 to 855 Ϯ 211 grams ϫ mm/min). LVH dogs showed no decrement in work as a result of treatment with SIN-1. L-NAME did not cause significant changes in myocardial cyclic GMP, O 2 consumption, or work in either control or LVH dogs, but vascular effects were evident. SIN-1 increased cyclic GMP, and with greater effect on LVH; however, this resulted in a decrement in function only in the control group. The greater increased cyclic GMP in LVH dogs is not related to increased NO production, but is related to significantly higher sensitivity and maximal activity of soluble myocardial guanylate cyclase.

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“…Candoxatrilat alone (3 and 10 mg kg-') had no effect on blood pressure when compared to vehicle-treated rats ( (Lattion et al, 1986;Brown et al, 1993). A small proportion of rats fail to compensate for the shunt and die in the first week post-surgery with sodium retention, manifest as pulmonary oedema and _ ascites (Winaver et al, 1988 .…”

Section: A -V Fistula Ratsmentioning

confidence: 99%

Renal effects of concurrent E‐24.11 and ACE inhibition in the aorto‐venocaval fistula rat

Kirk¹,

Wilkins²

1996

British J Pharmacology

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1 The present studies compare the early renal response to (a) an endopeptidase-24.11 (E-24.11) inhibitor (candoxatrilat) (b) an angiotensin-converting enzyme (ACE) inhibitor (lisinopril) and (c) the combination of endopeptidase-24.11 and ACE inhibition in the rat A-V fistula model of chronic volume overload. 2 Candoxatrilat (3 and 10 mg kg-') i.v. produced a prompt 3 fold increase in urinary sodium and cyclic GMP excretion without affecting significantly blood pressure or glomerular filtration rate (GFR).3 Lisinopril (0.03 mg kg-') alone inhibited the pressor response to angiotensin I but had no significant effect on urinary sodium excretion or blood pressure.4 Lisinopril (0.03 mg kg-') attenuated significantly the early natriuretic response to candoxatrilat (3 mg kg-1) and the associated rise in urinary cyclic GMP, but sodium excretion eventually reached levels associated with acute E-24.11 inhibition. 5 Doses of the dual E-24. 11/ACE inhibitor, sampatrilat, that inhibited the pressor response to angiotensin I reduced mean arterial blood pressure and produced a delayed natriuresis and rise in urinary cyclic GMP excretion when compared to candoxatrilat alone. 6 Concurrent administration of an ACE inhibitor reduces the early renal response to E-24.11 inhibition in the A-V fistula rat, an effect attributable to the hypotensive action of this combination.

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Differential regulation of natriuretic peptide receptor messenger RNAs during the development of cardiac hypertrophy in the rat.

Cited by 74 publications

References 86 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

Increased guanylate cyclase activity is associated with an increase in cyclic guanosine 3',5'-monophosphate in left ventricular hypertrophy.

Renal effects of concurrent E‐24.11 and ACE inhibition in the aorto‐venocaval fistula rat

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