scholarly journals Phosphorylation of the Small Heat Shock-related Protein, HSP20, in Vascular Smooth Muscles Is Associated with Changes in the Macromolecular Associations of HSP20

1999 ◽  
Vol 274 (10) ◽  
pp. 6324-6329 ◽  
Author(s):  
Colleen M. Brophy ◽  
Mary Dickinson ◽  
David Woodrum
Keyword(s):  
Heat Shock ◽  
Smooth Muscles ◽  
Related Protein ◽  
Vascular Smooth Muscles

Parathyroid hormone-related protein-(1-34) inhibits intrinsic pump activity of isolated murine lymph vessels

2001 ◽  
Vol 281 (1) ◽  
pp. H60-H66 ◽  
Author(s):  
Risuke Mizuno ◽  
Nobuyuki Ono ◽  
Toshio Ohhashi
Keyword(s):  
Parathyroid Hormone ◽  
Smooth Muscles ◽  
Related Protein ◽  
Vascular Smooth Muscles ◽  
Lymph Vessels ◽  
Parathyroid Hormone Related Protein ◽  
Low Concentrations ◽  
Pump Activity ◽  
Endogenous Nitric Oxide ◽  
High Concentrations

Parathyroid hormone-related protein (PTHrP) was originally found as a tumor-derived vasoactive factor and has also been known to produce significant relaxation of vascular smooth muscles. Thus effects of PTHrP-(1-34), a PTH receptor-binding domain, on spontaneous lymphatic pump activity was investigated in isolated pressurized lymph vessels of mice. Low concentrations (1 × 10−10 and 3 × 10−10 M) of PTHrP-(1-34) dilated lymph vessels and reduced the frequency of pump activity, whereas high concentrations (1 × 10−9 to 1 × 10−8 M) of PTHrP-(1-34) caused dilation with cessation of the lymphatic pump activity. N ω-nitro-l-arginine methyl ester (l-NAME; 3 × 10−5 M) but not indomethacin (1 × 10−5 M) significantly reduced the PTHrP-(1-34)-induced inhibitory responses of the lymphatic pump activity. In the presence of l-NAME (3 × 10−5 M) and l-arginine (1 × 10−3 M), the l-NAME-induced inhibition in the PTHrP-(1-34)-mediated responses was significantly reduced. Glibenclamide (1 × 10−6 M) significantly suppressed the inhibitory responses of the lymphatic pump activity induced by PTHrP-(1-34) and S-nitroso- N-acetyl-penicillamine. The PTHrP-(1-34)-mediated inhibitory responses were significantly reduced by treatment with PTHrP-(7-34) (1 × 10−7 M). These results suggest that PTHrP-(1-34) inhibits spontaneous pump activity of the isolated lymph vessels via PTH receptors and that production and release of endogenous nitric oxide and activation of ATP-sensitive K+ channels in the lymph vessels contribute to the PTHrP-(1-34)-mediated inhibitory responses of the lymphatic pump activity.

Effects of Sodium Vanadate on Various Types of Vascular Smooth Muscles

1986 ◽  
Vol 23 (3) ◽  
pp. 113-124 ◽  
Author(s):  
Tomoko Shimada ◽  
Keiichi Shimamura ◽  
Satoru Sunano
Keyword(s):  
Smooth Muscles ◽  
Vascular Smooth Muscles ◽  
Sodium Vanadate

scholarly journals Effects of Telmisartan on Myocardial Protein Profiles in Hypertensive Rats

2021 ◽  
Vol 34 (3) ◽  
pp. 299-299
Author(s):  
Yu Feng ◽  
Man-li Zhou ◽  
Jian-zhang Wang ◽  
Jia-qi Zhang ◽  
Shu-le Qian ◽  
...  
Keyword(s):  
Heat Shock ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Sterile Water ◽  
Protein Profiles ◽  
Related Protein ◽  
Hypertensive Rats ◽  
Treatment Groups ◽  
Proteasome 26S

Abstract Background To investigate the effects of telmisartan on the protein profiles of the left ventricular myocardium in spontaneously hypertensive rats (SHR). Methods Sixteen SHR were randomly divided into control and telmisartan treatment groups. Rats were treated with sterile water (10 ml/kg) or telmisartan (4.33 mg/kg) by gavage for 12 weeks. Wistar-Kyoto (WKY) rats treated with sterile water (10 ml/kg) as controls. At the end of 12 weeks of control or telmisartan treatment, rats were sacrificed, and hearts were collected for protein preparations, isotope labeling, and mass spectrometric analysis. Results In total, there were 23 differentially expressed proteins in the left ventricular myocardium between control and telmisartan treatment groups in SHR. Compared with the telmisartan group, the upregulated proteins in the SHR were dual-specificity mitogen-activated protein kinase kinase 3-like, transgelin, and haptoglobin subtype 2. The downregulated proteins in the SHR were as follows: von Willebrand factor (fragment), kininogen 1, small ribonucleoprotein-related protein, fibrinogen beta chain, protein mass 3 (fragment), proteasome 26s, heat shock protein 27-related protein 1, tenascin X, fibronectin subtype 2, transferrin receptor protein, platelets 1, cathepsin L1, complement factor B, isoform CRA_b, fibrinogen isomer, immunoglobulin heavy chain (γ polypeptide), and α 1 antiprotease. Conclusions Telmisartan differentially regulates myocardial protein expression in hypertensive rats including heat shock protein 27, fibrinogen, fibronectin, proteasome 26s and transgelin, as well as proteins in biochemical, metabolic, and signal transduction pathways. These changes in protein expression may contribute to the antihypertrophic effects of telmisartan in hypertension.

scholarly journals Modeling of the Bayliss‐Effect in Vascular Smooth Muscles

PAMM ◽  
2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Klemens Uhlmann ◽  
Daniel Balzani
Keyword(s):  
Smooth Muscles ◽  
Vascular Smooth Muscles ◽  
Bayliss Effect

Plasticity of KIR channels in human smooth muscle cells from internal thoracic artery

2003 ◽  
Vol 284 (6) ◽  
pp. H2325-H2334 ◽  
Author(s):  
Tom Karkanis ◽  
Shaohua Li ◽  
J. Geoffrey Pickering ◽  
Stephen M. Sims
Keyword(s):  
Smooth Muscle ◽  
Current Density ◽  
Internal Thoracic Artery ◽  
Smooth Muscles ◽  
Vascular Smooth Muscles ◽  
Rt Pcr ◽  
Regulation Of Proliferation ◽  
Negative Membrane Potential ◽  
Inwardly Rectifying ◽  
Contractile Cells

Inwardly rectifying K+ (KIR) currents are present in some, but not all, vascular smooth muscles. We used patch-clamp methods to examine plasticity of this current by comparing contractile and proliferative phenotypes of a clonal human vascular smooth muscle cell line. Hyperpolarization of cells under voltage clamp elicited a large inward current that was selective for K+ and blocked by Ba2+. Current density was greater in proliferative compared with contractile cells (−4.5 ± 0.9 and −1.4 ± 0.3 pA/pF, respectively; P < 0.001). RT-PCR of mRNA from proliferative cells identified transcripts for Kir2.1 and Kir2.2 but not Kir2.3 potassium channels. Western blot analysis demonstrated greater expression of Kir2.1 protein in proliferative cells, consistent with the higher current density. Proliferative cells displayed a more negative membrane potential than contractile cells (−71 ± 2 and −35 ± 4 mV, respectively; P < 0.001). Ba2+ depolarized all cells, whereas small increases in extracellular K+ concentration elicited hyperpolarization only in contractile cells. Ba2+ inhibited [3H]thymidine incorporation, indicating a possible role for KIR channels in the regulation of proliferation. The phenotype-dependent plasticity of KIR channels may have relevance to vascular remodeling.

scholarly journals Hypercapnic Acidosis Activates K ATP Channels in Vascular Smooth Muscles

2003 ◽  
Vol 92 (11) ◽  
pp. 1225-1232 ◽  
Author(s):  
Xueren Wang ◽  
Jianping Wu ◽  
Li Li ◽  
Fuxue Chen ◽  
Runping Wang ◽  
...  
Keyword(s):  
Smooth Muscles ◽  
Hypercapnic Acidosis ◽  
Vascular Smooth Muscles

scholarly journals Rhythmic contraction generates adjustable passive stiffness in rabbit detrusor

2010 ◽  
Vol 108 (3) ◽  
pp. 544-553 ◽  
Author(s):  
Atheer M. Almasri ◽  
Paul H. Ratz ◽  
Hersch Bhatia ◽  
Adam P. Klausner ◽  
John E. Speich
Keyword(s):  
Kinase Inhibitor ◽  
Smooth Muscles ◽  
Physiological Role ◽  
Passive Tension ◽  
Passive Stiffness ◽  
Vascular Smooth Muscles ◽  
Rhythmic Contraction ◽  
Length Changes ◽  
Changes Over Time ◽  
Adjustable Passive Stiffness

The length-tension ( L-T) relationships in airway and vascular smooth muscles have been shown to adapt with length changes over time. Our prior studies have shown that the active and passive L-T relationships in rabbit detrusor smooth muscle (DSM) can adapt and that DSM exhibits adjustable passive stiffness (APS) characterized by a passive L-T curve that is a function of strain and activation history. The present study demonstrates that passive tension due to APS can represent a substantial fraction of total tension over a broad length range. Our previous studies have shown that maximal KCl-induced contractions at short muscle lengths generate APS that is revealed by increased pseudo-steady-state passive tension at longer lengths compared with previous measurements at those lengths. The objective of the present study was to determine the mechanisms involved in APS generation. Increasing the number of KCl-induced contractions or the duration of a contraction increased the amount of APS generated. Furthermore, a fraction of APS was restored in calcium-free solution and was sensitive to the general serine and threonine protein kinase inhibitor staurosporine. Most importantly, rhythmic contraction (RC) generated APS, and because RC occurs spontaneously in human bladder, a physiological role for RC was potentially identified.

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