atrial-natriuretic-factor and Vascular-Diseases

The Natriuretic Peptide (NP) family, especially its best-characterized member Atrial Natriuretic Peptide (ANP), plays an important role in the regulation of blood pressure homeostasis and salt and water balance. Besides their action in cardiovascular physiology, NPs have been described as anti-inflammatory regulators of macrophage function: they have been reported to inhibit the induction of inflammatory mediators, such as iNOS, COX-2, and TNF-alpha. In the following review we will focus on a rather novel aspect of NP action: NPs, especially ANP, will be presented as vasoprotective agents. We will specifically focus on ANP's interaction with the complex intracellular signalling networks responsible for proliferation, vascular permeability, attraction and adhesion of leukocytes, and the induction of cytoprotective proteins. We will also discuss the critical mediator systems involved in mediating ANP's beneficial actions. Recently, ANP as well as BNP, another member of the NP family, have been introduced as cardiovascular therapeutics. In this context, we will highlight the physiological and pharmacological relevance of NPs, particularly ANP, as endogenous vasoprotective agents.

Topics: Animals; Atrial Natriuretic Factor; Capillary Permeability; Cyclic GMP; Cytoprotection; Endothelial Cells; Heat-Shock Proteins; Humans; Leukocyte Disorders; Natriuretic Peptides; Second Messenger Systems; Tumor Necrosis Factor-alpha; Vascular Diseases

Topics: Animals; Atrial Natriuretic Factor; Blood Vessels; Genetic Therapy; Humans; Rats; Vascular Diseases

Topics: Animals; Atrial Natriuretic Factor; Cardiac Output; Head-Down Tilt; Natriuretic Peptide, Brain; Rats; Rats, Sprague-Dawley; Regional Blood Flow; Vascular Diseases; Vascular Resistance; Vasoconstriction; Veins; Weightlessness Simulation

The important role of atrial natriuretic peptides (ANP) in regulating blood pressure and changing vascular permeability has been widely studied and assessed during the last ten years. Considering the characteristics of this mechanism, which is responsible for a hypotensive and hypovolemic effect, and the possible role of hypotension associated with a default of autoregulatory sympathetic reactions in inner ear unexplained disorders, it seems reasonable to hypothesize a possible involvement of ANP system in the genesis of such disorders. As a matter of fact, the presence of specific receptors for ANP in the inner ear has been widely reported in studies concerning both rat and human inner ear, although their precise role in the labyrinthine homeostasis has not been satisfactory explained until now. Some aspects concerning vascular and fluid regulation of the inner ear under different conditions still remain not totally clear, and consequently a detailed explanation to the possible mechanism causing inner ear disorders of functional origin is lacking; from this point of view, an investigation on the serum level of ANP in subjects with labyrinthine affections of uncertain origin could be of some utility in contributing to assess the role of this system in the inner ear fluid regulation and in the inner ear perfusion and to investigate on the possible influence of an abnormal ANP release in some kind of inner ear damage.

Topics: Atrial Natriuretic Factor; Ear, Inner; Humans; Labyrinth Diseases; Microcirculation; Models, Biological; Vascular Diseases

Increased arterial compliance (COMPart) has recently been described in patients with cirrhosis, particularly in advanced disease. The aim of the present study was to relate COMPart with arterial levels of the circulating natriuretic peptides: atrial natriuretic peptide (ANP) and C-type natriuretic peptide (CNP), both of which are vasodilators.. Thirty-one patients with cirrhosis, 14 non-cirrhotic patients with circulatory disturbances of the ischaemic and hypertensive type, and 10 healthy controls were investigated during a haemodynamic examination.. The patients with cirrhosis showed the well-known hyperdynamic circulation with elevated cardiac output, low arterial blood pressure, and reduced systemic vascular resistance. COMPart in the patients with cirrhosis (1.30 mL/mmHg) was significantly (P < 0.01) increased compared to that of non-cirrhotic patients (0.99 mL/mmHg) and controls (1.01 mL/mmHg). In the patients with cirrhosis, a significant inverse correlation was found between CNP and COMPart (r = -0.42, P < 0.01), but not between CNP and systemic vascular resistance (r = 0.31, P = 0.08). In the non-cirrhotic patients, CNP had a significant inverse correlation to COMPart (r = -0.68, P < 0.01) and a direct correlation to systemic vascular resistance (r = 0.62, P < 0.02). ANP was not significantly related to COMPart nor to systemic vascular resistance in any of the groups.. The finding of an inverse relation between CNP and COMPart may suggest that a compensatory down-regulation of CNP occurs in patients with cirrhosis and other types of circulatory disorders when vasodilation persists. Regulation of large and small arteries by CNP may be different in cirrhosis. Arterial ANP is not related to properties of the large or small arteries.

Topics: Adult; Aged; Arteries; Atrial Natriuretic Factor; Dilatation, Pathologic; Female; Hemodynamics; Humans; Liver Cirrhosis; Male; Middle Aged; Natriuretic Peptide, C-Type; Vascular Diseases

Primary prevention of cardiovascular disease has been aimed at risk factor identification and treatment without efforts to document early cardiovascular disease. The objective of the current study is to screen individuals with vascular and cardiac tests aimed at identifying early abnormalities likely to progress and to measure risk contributors susceptible to therapy.. A center was established for comprehensive screening of an asymptomatic population with 10 tests designed to detect early vascular and cardiac abnormalities and blood tests to identify potential targets for risk contributor intervention. The first 396 individuals screened in the center have been analyzed.. Using a scoring system from 0 (no disease) to 20 (advanced disease), 49% of the population exhibited scores of > or =5 and 39% exhibited scores of > or =6. These scores appear indicative of early disease mandating initiation of or change in medical therapy, which was recommended to the individuals screened and to their primary care physicians.. The screening tests utilized are effective in uncovering unsuspected early cardiovascular disease in which targeted treatment could be effective in reducing the incidence of cardiovascular events in susceptible individuals. Documentation of the sensitivity and specificity of this approach requires longitudinal study.

Topics: Adult; Aged; Arteries; Atrial Natriuretic Factor; Biomarkers; Blood Pressure Determination; Echocardiography; Elasticity; Electrocardiography; Female; Fundus Oculi; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Risk Factors; Sex Factors; Systole; Vascular Diseases; Ventricular Dysfunction, Left

Lysophosphatidylcholine (LPC), a major atherogenic lysophospholipid contained in oxidized low-density lipoprotein (ox-LDL), induces endothelial dysfunction. Recent studies showed that natriuretic peptides (NPs) have antiatherogenic properties by inhibiting vascular smooth-muscle cell proliferation, but their effects on endothelial cells are little known. We examined whether atrial and brain NPs (ANP and BNP) have a protecting action against LPC-induced endothelial dysfunction. LPC (10 microM) significantly inhibited thrombin (0.001-1 U/ml)-induced endothelium-dependent relaxation without affecting endothelium-independent relaxation to sodium nitroprusside in isolated porcine coronary arteries. The impaired endothelium-dependent relaxation induced by LPC was prevented by treatment with ANP or BNP (i microM). In cultured bovine aortic endothelial cells (BAECs), LPC (10 microM) significantly attenuated bradykinin (1 microM)-stimulated nitric oxide (NO) release; however, this was prevented by ANP and BNP. Because LPC-induced endothelial dysfunction has been shown to be mediated at least in part by activation of the protein kinase C (PKC)-dependent signaling pathway, we also examined the effects of ANP and BNP on LPC-induced modulation of PKC activities in BAECs. LPC (10 microM) significantly stimulated PKC activity in BAECs. However, ANP or BNP significantly inhibited LPC (10 microM)-induced PKC activation. In conclusion, ANP and BNP protected endothelial cells from LPC-induced dysfunction in both isolated coronary arteries and cultured ECs. The mechanism appears to be at least in part related to the inhibition of LPC-induced PKC activation by NPs. These new actions of ANP and BNP against lysolipid-induced endothelial cytotoxicity may partly account for antiatherogenic properties of NPs.

Topics: 8-Bromo Cyclic Adenosine Monophosphate; Animals; Atrial Natriuretic Factor; Cattle; Coronary Vessels; Dinoprost; Endothelium, Vascular; Enzyme Activation; In Vitro Techniques; Lysophosphatidylcholines; Muscle Relaxation; Muscle, Smooth, Vascular; Natriuretic Peptide, Brain; Nitrates; Nitric Oxide; Nitrites; Protein Kinase C; Signal Transduction; Swine; Vascular Diseases

Chronic constriction of the thoracic inferior vena cava results in decreased filling pressure and cardiac output, in augmented secretion rates of renin and aldosterone, and in marked sodium retention with ascites and edema formation. The goal of the present study was to determine temporal changes in the plasma concentration of immunoreactive atrial natriuretic factor (iANF) in response to chronic constriction of the thoracic inferior vena cava in the conscious dog. Following constriction of the thoracic inferior vena cava, all dogs retained sodium avidly for at least 10 days, and both plasma renin activity and plasma aldosterone concentration increased markedly (p less than 0.05). Additionally, the baseline plasma iANF of 70 +/- 5 pg/ml decreased significantly to 24 +/- 7, 26 +/- 10, and 34 +/- 11 pg/ml (p less than 0.05) on days 2, 6, and 10 following thoracic inferior vena cava constriction. Thus, chronic sodium retention in this model is associated with prolonged endocrine adjustments in the circulating levels of renin-aldosterone and iANF. We suggest that chronic decreases in the secretion of atrial natriuretic factor might contribute to the inability of the dog with constriction of the thoracic inferior vena cava to excrete sodium normally.

Topics: Animals; Atrial Natriuretic Factor; Central Venous Pressure; Constriction, Pathologic; Dogs; Female; Natriuresis; Osmolar Concentration; Vascular Diseases; Vena Cava, Inferior