scholarly journals Insulin increases cyclic nucleotide content in human vascular smooth muscle cells: a mechanism potentially involved in insulin-induced modulation of vascular tone

Diabetologia ◽  
1995 ◽  
Vol 38 (8) ◽  
pp. 936-941
Author(s):  
M. Trovati ◽  
P. Massucco ◽  
L. Mattiello ◽  
F. Cavalot ◽  
E. Mularoni ◽  
...  
2000 ◽  
Vol 6 (S2) ◽  
pp. 598-599
Author(s):  
J. Lin ◽  
C. Wei

Brain natriuretic peptide (BNP) is a peptide of cardiac origin which regulates plasma volume as well as vascular tone and growth. Recently, we have reported that brain natriuretic peptide is a potent inhibitor of endothelin-1-mediated proliferation in human coronary vascular smooth muscle cells (HCoVSMC). While brain natriuretic peptide has been reported to be produced and released from atrial and ventricular myocardium, we hypothesize that brain natriuretic peptide may be present and secreted from human coronary vascular smooth muscle cells.Therefore, the present study was designed to investigate the secretion of brain natriuretic peptide in cultured human coronary vascular smooth muscle cells (HCoVSMC: Clonetics, San Diego, CA). The concentration of brain natriuretic peptide, and its second messenger cGMP, in culture media (48 hours) was determined by radioimmunoassay (Phoenix, Mountain View, CA). The presence of brain natriuretic peptide was determined by immunohistochemical staining using a human brain natriuretic peptide polyclonal antibody.


2021 ◽  
Vol 9 (1) ◽  
pp. 4
Author(s):  
Margarida Lorigo ◽  
Nelson Oliveira ◽  
Elisa Cairrao

Cardiovascular diseases are important causes of mortality and morbidity worldwide. Vascular smooth muscle cells (SMCs) are major components of blood vessels and are involved in physiologic and pathophysiologic conditions. In healthy vessels, vascular SMCs contribute to vasotone and regulate blood flow by cyclic nucleotide intracellular pathways. However, vascular SMCs lose their contractile phenotype under pathological conditions and alter contractility or signalling mechanisms, including cyclic nucleotide compartmentation. In the present review, we focus on compartmentalized signaling of cyclic nucleotides in vascular smooth muscle. A deeper understanding of these mechanisms clarifies the most relevant axes for the regulation of vascular tone. Furthermore, this allows the detection of possible changes associated with pathological processes, which may be of help for the discovery of novel drugs.


2020 ◽  
Vol 21 (14) ◽  
pp. 5160 ◽  
Author(s):  
Nadine Wehbe ◽  
Suzanne Awni Nasser ◽  
Yusra Al-Dhaheri ◽  
Rabah Iratni ◽  
Alessandra Bitto ◽  
...  

Vascular smooth muscle cells (VSMCs) are major components of blood vessels. They regulate physiological functions, such as vascular tone and blood flow. Under pathological conditions, VSMCs undergo a remodeling process known as phenotypic switching. During this process, VSMCs lose their contractility and acquire a synthetic phenotype, where they over-proliferate and migrate from the tunica media to the tunica interna, contributing to the occlusion of blood vessels. Since their discovery as effector proteins of cyclic adenosine 3′,5′-monophosphate (cAMP), exchange proteins activated by cAMP (EPACs) have been shown to play vital roles in a plethora of pathways in different cell systems. While extensive research to identify the role of EPAC in the vasculature has been conducted, much remains to be explored to resolve the reported discordance in EPAC’s effects. In this paper, we review the role of EPAC in VSMCs, namely its regulation of the vascular tone and phenotypic switching, with the likely involvement of reactive oxygen species (ROS) in the interplay between EPAC and its targets/effectors.


1988 ◽  
Vol 255 (2) ◽  
pp. C169-C180 ◽  
Author(s):  
M. E. O'Donnell ◽  
N. E. Owen

We have previously demonstrated the presence of a prominent, cyclic nucleotide-sensitive Na-K-Cl cotransport in vascular smooth muscle cells (VSMC). Others have observed that Na-K-Cl cotransport levels are reduced in erythrocytes of patients with essential hypertension and have proposed that a defect in this Na transport system may play a role in the pathogenesis of the disease. However, such a defect has not been demonstrated in the putative target tissue for essential hypertension, i.e., the VSMC. In the present study, we compared Na-K-Cl cotransport of VSMC from spontaneously hypertensive rats (SHR) with Na-K-Cl cotransport of VSMC from normotensive Wistar-Kyoto rats (WKY). We found that Na-K-Cl cotransport of SHR VSMC is significantly reduced relative to that of WKY VSMC (3.09 vs. 4.39 mumol K.g protein-1.min-1). The apparent ion affinities for Na-K-Cl cotransport of SHR VSMC did not differ from those determined for WKY VSMC. Furthermore, cyclic nucleotide regulation of cotransport also appeared to be the same for the two types of VSMC. In contrast, maximal saturable binding of [3H]bumetanide observed in SHR VSMC was markedly reduced compared with that of WKY VSMC, but the Kd values were similar. Our data suggest that the reduction in cotransport observed in SHR VSMC is the result of a decrease in the number of available cotransport sites.


2019 ◽  
Vol 176 (11) ◽  
pp. 1780-1792 ◽  
Author(s):  
Liang Zhang ◽  
Kaouter Bouadjel ◽  
Boris Manoury ◽  
Grégoire Vandecasteele ◽  
Rodolphe Fischmeister ◽  
...  

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