Wyniki wyszukiwania

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Natriuretic peptides reduce plasminogen activator inhibitor-1 expression in human endothelial cells

100%

Pawlowska Z., Jerczynska H., Szemraj J., Baranska P., Swiatkowska M., Cierniewski C. S.

Cellular and Molecular Biology Letters

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2002

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tom 07

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nr 4

Plasma concentrations of natriuretic peptides increase in some pathological conditions, but very little is known about the effect of these vasodilator peptides on the regulation of the blood coagulation system. The fundamental role in the regulation of fibrinolysis is played by plasminogen activator inhibitor type 1 (PAI-1). Recent studies demonstrate that natriuretic peptides can modulate PAI-1 expression in bovine aortic smooth muscle cells and rat aortic endothelial cells. In this report, we tested the effect of natriuretic peptides on PAI-1 expression in the human endothelial cell line (EA.hy 926). For this purpose, we treated the cell cultures with ANP, BNP and CNP, and modulation of PAI-1 synthesis was evaluated. We compared the effect of natriuretic peptides on synthesis and release of PAI-1 in unstimulated cells, and after activation with tumour necrosis factor α (TNFα). Natriuretic peptides abolished TNFα-induced upregulation of PAI-1 expression at both the PAI-1 mRNA and the antigen levels. The inhibitory efficiency was higher in the case of CNP when compared to that produced by ANP and BNP, particularly when TNFα-stimulated cells were used. We observed an inhibition of stimulatory effect of TNFα on PAI-1 expression also at the level of the PAI-1 promoter in cells transfected with a PAI-1 promoter fragment (+71 to -800) [1], The PAI-1 promoter activity was markedly inhibited by C-type natriuretic peptide, already at a very low (0.001 µM) concentration of the peptide.

2

Atrial natiuretic peptide and brain natriuretic peptide changes after epicardial percutaneous left atrial appendage suture ligation using LARIAT device

63%

Bartus K., Podolec J., Lee R. J., Kapelak B., Sadowski J., Bartus M., Oles K., Ceranowicz P., Trabka R., Litwinowicz R.

Journal of Physiology and Pharmacology

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2017

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tom 68

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nr 1

3

Cyclic GMP metabolism and its role in brain physiology

63%

Domek-Lopacinska K., Strosznajder J. B.

Journal of Physiology and Pharmacology. Supplement

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2005

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tom 56

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nr 2

15-34

Cyclic GMP (cGMP) is synthesized by guanylyl cyclase (GC) in response to nitric oxide (NO) and carbon monoxide (CO) or natiuretic peptides (NPs); atrial, brain and C-type (ANP, BNP and CNP). cGMP is degraded by several cGMP-specific phosphodiesterases (PDEs). Guanylate cyclases (GC) are differentiated into: membrane-bound/particulate (pGC) and cytosolic/soluble (sGC). In recent years evidence has accumulated that NO is the main activator of sGC and NO/cGMP plays important role in glutaminergic, cholinergic and dopaminergic signaling pathways. cGMP in the nervous system is involved in long term potentiation and depression (LTP, LTD) suggesting its participation in learning and memory mechanism. cGMP regulates calcium homeostasis and phototransduction. Its level is regulated by PDEs and their specific inhibitors protect cGMP level in cells and are very important from clinical point of view.

4

Regulation of cGMP synthesis in cultured podocytes by vasoactive hormones

63%

Lewko B., Golos M., Latawiec E., Angielski S., Stepinski J.

Journal of Physiology and Pharmacology

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2006

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tom 57

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nr 4

The podocytes are highly differentiated cells playing a key role in glomerular filtration. Vasoactive factors including angiotensin II (Ang II) and cyclic guanosine 5' monophosphate (cGMP) are synthesized by these cells upon stimulation as well as in the basal state. In this study we have tested whether angiotensin II affects the total synthesis of cGMP in primary culture of rat podocytes. The cells were stimulated with atrial natriuretic peptide (ANP) and/or a nitric oxide (NO) donor, S-nitroso-N-acetyl penicillamine (SNAP), in the absence or presence of Ang II. The cGMP synthesis was determined by radioimmunoassay (RIA). ANP or SNAP alone increased the cGMP synthesis in podocytes although the effects were not additive unless Ang II was present in the medium. Ang II suppressed the ANP-dependent cGMP synthesis whereas SNAP-dependent cGMP production remained unaffected. These effects were prevented by a non-specific antagonist of Ang II receptors (AT), saralasin. Adversely, PD123319, a specific inhibitor of AT2 receptors, augmented inhibition of ANP-dependent and enhanced the NO-dependent cGMP production. Probenecid, an inhibitor of cGMP extrusion from the cells, suppressed the cGMP generation by both ANP and SNAP. We conclude that cGMP synthesis in cultured podocytes is modulated by angiotensin II and that two adversely acting receptors, AT1 and AT2 are involved in this effect. Additionally, production of cGMP might be intrinsically inhibited by cGMP accumulating inside the cells.

5

Natriuretic peptides in cardiovascular diseases

51%

Piechota M., Banach M., Jacon A., Rysz J.

Cellular and Molecular Biology Letters

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2008

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tom 13

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nr 2

155-181

The natriuretic peptide family comprises atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), C-type natriuretic peptide (CNP), dendroaspis natriuretic peptide (DNP), and urodilatin. The activities of natriuretic peptides and endothelins are strictly associated with each other. ANP and BNP inhibit endothelin-1 (ET-1) production. ET-1 stimulates natriuretic peptide synthesis. All natriuretic peptides are synthesized from polypeptide precursors. Changes in natriuretic peptides and endothelin release were observed in many cardiovascular diseases: e.g. chronic heart failure, left ventricular dysfunction and coronary artery disease.

6

Blood specimen biomarkers of inflammation, matrix degradation, angiogenesis, and cardiac involvement: a future useful tool in assessing clinical outcomes of COPD patients in clinical practice?

51%

Kristan S. S.

Archivum Immunologiae et Therapiae Experimentalis

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2013

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tom 61

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nr 6

7

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The mechanism of Naplus, Kplus -ATPase inhibition by atrial natriuretic factor in rat renal medulla

51%

Beltowski J., Gorny D., Marciniak A.

Journal of Physiology and Pharmacology

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1998

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tom 49

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nr 2

8

Physiology and pathophysiology of vascular signalling controlled by guanosine 3',5'-cyclic monophosphate-dependent protein kinase

51%

Birschmann I., Walter U.

Acta Biochimica Polonica

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2004

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tom 51

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nr 2

Recent medical advances suggest that the cellular natriuretic peptide/cGMP and NO/cGMP effector systems represent important signal transduction pathways especially in the cardiovascular system. These pathways also appear to be very interesting targets for the possible prevention of cardiovascular diseases. Exciting candidates for prevention include cGMP-dependent signaling networks initiated by natriuretic peptides (NP) and nitric oxide (NO) which are currently explored for their diagnostic and therapeutic potential. cGMP signaling contributes to the function and interaction of several vascular cell types, and its dysfunction is involved in the progression of major cardiovascular diseases such as atherosclerosis, hypertension and diabetic complications. This review will take a focussed look at key elements of the cGMP signaling cascade in vascular tissue. Recent advances in our knowledge of cGMP-dependent protein kinases (cGK, also known as PKG), the potential for assessing the functional status of cGMP signaling and the possible cross talk with insulin signaling will be reviewed.

Ograniczanie wyników

Natriuretic peptides reduce plasminogen activator inhibitor-1 expression in human endothelial cells

Atrial natiuretic peptide and brain natriuretic peptide changes after epicardial percutaneous left atrial appendage suture ligation using LARIAT device

Cyclic GMP metabolism and its role in brain physiology

Regulation of cGMP synthesis in cultured podocytes by vasoactive hormones

Natriuretic peptides in cardiovascular diseases

Blood specimen biomarkers of inflammation, matrix degradation, angiogenesis, and cardiac involvement: a future useful tool in assessing clinical outcomes of COPD patients in clinical practice?

The mechanism of Naplus, Kplus -ATPase inhibition by atrial natriuretic factor in rat renal medulla

Physiology and pathophysiology of vascular signalling controlled by guanosine 3',5'-cyclic monophosphate-dependent protein kinase