Role of Natriuretic Peptide Family in Cardiovascular Medicine

Das, Bibhuti B.; Solinger, Robert

doi:10.2174/187152509787047630

Cited by 20 publications

(16 citation statements)

References 136 publications

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“…While activation of the renin-angiotensin-aldosterone system causes sodium retention, sodium excretion is controlled by several natriuretic factors [252]. These factors include a number of natriuretic peptides such as the atrial natriuretic peptide, and the B-type and C-type natriuretic peptides [253]. Natriuretic peptides are primarily synthesised in the heart and brain.…”

Section: Copd and Renin-angiotensin-aldosterone Systemmentioning

confidence: 99%

Endocrinological derangements in COPD

Laghi

Adıgüzel²,

Tobin³

2009

European Respiratory Journal

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Chronic obstructive pulmonary disease (COPD) is no longer considered to affect only the lungs and airways but also the rest of the body. The systemic manifestations of COPD include a number of endocrine disorders, such as those involving the pituitary, the thyroid, the gonads, the adrenals and the pancreas.The mechanisms by which COPD alters endocrine function are incompletely understood but likely involve hypoxaemia, hypercapnia, systemic inflammation and glucocorticoid administration. Altered endocrine function can worsen the clinical manifestations of COPD through several mechanisms, including decreased protein anabolism, increased protein catabolism, nonenzymatic glycosylation and activation of the rennin-angiotensin-aldosterone system.Systemic effects of endocrine disorders include abnormalities in control of breathing, decreases in respiratory and limb-muscle mass and function, worsening of respiratory mechanics, impairment of cardiac function and disorders of fluid balance.Research on endocrine manifestations of COPD embraces techniques of molecular biology, integrative physiology and controlled clinical trials. A sound understanding of the various disorders of endocrine function associated with COPD is prudent for every physician who practices pulmonary medicine.

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Section: Copd and Renin-angiotensin-aldosterone Systemmentioning

confidence: 99%

Endocrinological derangements in COPD

Laghi

Adıgüzel²,

Tobin³

2009

European Respiratory Journal

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“…CNP is widely expressed along the vascular bed and is highly expressed in endothelium where is stored and plays an important role by inducing vasorelaxation in large conduction vessels through activation of NPR-B receptor subtype [12]. As a vasodilator agent, CNP inhibits the release of endothelin stimulated by angiotensin II (Ang II) [15]. CNP can also activate NPR-C receptor that leads to an hyperpolarizing effect in resistance vascular bed, suggesting that CNP acts as an endothelium derived hyperpolarizing factor (EDHF) together with other paracrine endothelial vasorelaxant mediators such as nitric oxide (NO) and prostacyclin [2,13,16,17].…”

Section: Cnp and The Cardiovascular Systemmentioning

confidence: 99%

“…The expression of CNP in injured arterial vessels stimulates inducible nitric oxide synthase secretion leading to NO production [14]. It also inhibits angiotensin I vasoconstrictive effect but not that of Ang II, suggesting that CNP may exert local endogenous regulatory actions on vascular angiotensin converting enzyme (ACE) [14,15] (Figure 2).…”

Section: Cnp and The Cardiovascular Systemmentioning

confidence: 99%

Clinical Aspects of C-Type Natriuretic Peptide on the Cardiovascular System

R¹,

S²,

M³

et al. 2015

Int J Clin Endocrinol Metab

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C-type natriuretic peptide (CNP) is one of the three most important members of the human natriuretic peptide family, sharing with them a highly conserved 17-aminoacid ring structure, essential to elicit its biological actions by binding to its specific receptor NPR-B. CNP acts in a paracrine or autocrine way and it is cleared from plasma circulation by the NPR-C receptor. This is one of the reasons why its plasma levels are usually low. CNP is widely spread in human tissues, being localized in a variety of cells such as cardiac and vascular smooth muscle cells, chondrocytes, macrophages, glial cells, and renal, brain and reproductive tissues. In the cardiovascular system, CNP is stored in endothelial cells and exert different actions like vasodilation in large conduction vessels, and anti-proliferative, pro-apoptotic, anti-fibrotic and anti-hypertrophic properties in cardiomyocytes; it also inhibits neointimal restenosis and reduces cardiac ischemia-reperfusion injury and vascular constrictive remodeling. In addition, it has been suggested that CNP acts as an endothelium derived hyperpolarizing factor as a consequence of its hyperpolarizing action in resistance arterial smooth vessels muscle. Regarding its clinical aspects, it has been demonstrated the relation between CNP and different cardiovascular pathologies such as heart failure, myocardial infarction, cardiac remodeling, arterial hypertension, angiogenesis and revascularization, restenosis, atherosclerosis, pulmonary hypertension, and myocardial aging.

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“…In vitro studies show that corin, which is highly expressed in cardiac tissue [126], is able to convert the cellassociated inactive pro-ANP into its active form on the surface of cardiomyocytes [127,128]. ANP plays a key role in regulating blood pressure by regulating systemic salt and water balance [129,130]. Consistent with an in vivo role in this conversion, corin deficient mice show defects in the conversion of pro-ANP to ANP, and development of spontaneous hypertension and cardiac hypertrophy that is exacerbated by a high salt diet [131].…”

Section: Activation Of Natriuretic Peptidesmentioning

confidence: 99%

The cutting edge: membrane-anchored serine protease activities in the pericellular microenvironment

Antalis

Buzza

Hodge

et al. 2010

Biochemical Journal

134

153

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Synopsis The serine proteases of the trypsin-like (S1) family play critical roles in many key biological processes including digestion, blood coagulation, and immunity. Recent studies have identified members of this family which contain amino- or carboxy-terminal domains that serve to tether the serine protease catalytic domain directly at the plasma membrane. These membrane anchored serine proteases are proving to be key components of the cell machinery for activation of precursor molecules in the pericellular microenvironment, playing vital functions in the maintenance of homeostasis. Substrates activated by membrane anchored serine proteases include peptide hormones, growth and differentiation factors, receptors, enzymes, adhesion molecules and viral coat proteins. In addition, new insights into our understanding of the physiological functions of these proteases and their involvement in human pathology have come from animal models and patient studies. This review discusses emerging evidence for the diversity of this fascinating group of membrane serine proteases as potent modifiers of the pericellular microenvironment through proteolytic processing of diverse substrates. We also discuss the functional consequences of the activities of these proteases on mammalian physiology and disease.

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Role of Natriuretic Peptide Family in Cardiovascular Medicine

Cited by 20 publications

References 136 publications

Endocrinological derangements in COPD

Endocrinological derangements in COPD

Clinical Aspects of C-Type Natriuretic Peptide on the Cardiovascular System

The cutting edge: membrane-anchored serine protease activities in the pericellular microenvironment

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