scholarly journals Cyclic nucleotide signalling compartmentation by PDEs in cultured vascular smooth muscle cells

2019 ◽  
Vol 176 (11) ◽  
pp. 1780-1792 ◽  
Author(s):  
Liang Zhang ◽  
Kaouter Bouadjel ◽  
Boris Manoury ◽  
Grégoire Vandecasteele ◽  
Rodolphe Fischmeister ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Cyclic Nucleotide ◽  
Muscle Cells

scholarly journals PDE-Mediated Cyclic Nucleotide Compartmentation in Vascular Smooth Muscle Cells: From Basic to a Clinical Perspective

2021 ◽  
Vol 9 (1) ◽  
pp. 4
Author(s):  
Margarida Lorigo ◽  
Nelson Oliveira ◽  
Elisa Cairrao
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Cyclic Nucleotide ◽  
Muscle Cells ◽  
Mortality And Morbidity ◽  
Vascular Smcs ◽  
Novel Drugs ◽  
Causes Of Mortality

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.

Reduced Na-K-Cl cotransport in vascular smooth muscle cells from spontaneously hypertensive rats

1988 ◽  
Vol 255 (2) ◽  
pp. C169-C180 ◽  
Author(s):  
M. E. O'Donnell ◽  
N. E. Owen
Keyword(s):  
Smooth Muscle ◽  
Essential Hypertension ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Cyclic Nucleotide ◽  
Spontaneously Hypertensive Rats ◽  
Muscle Cells ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

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.

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