Contractile properties of isolated vascular smooth muscle after photoradiation

1989 ◽  
Vol 256 (3) ◽  
pp. H655-H664 ◽  
Author(s):  
W. Freas ◽  
J. L. Hart ◽  
D. Golightly ◽  
H. McClure ◽  
S. M. Muldoon
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Carotid Arteries ◽  
Laser Light ◽  
Ringer Solution ◽  
Vascular Effect ◽  
Laser Illumination ◽  
Vascular Physiology ◽  
Vascular Beds ◽  
Oxygen Derived Radicals

The purpose of this study was to characterize the responses of various types of vascular smooth muscle to conditions that would be encountered during photodynamic therapy, namely laser illumination of photosensitizer-pretreated tissue. Vascular smooth muscle obtained from representative canine, rodent, and rabbit vascular beds was cut into rings and placed in organ baths (37 degrees C, aerated with 95% O2-5% CO2). These vessels were pretreated for 30 min with the photosensitizer hematoporphyrin derivative (HpD, 3-30 micrograms/ml) washed, and then exposed to red laser light (633 nm, 1-3.5 mW) for up to 20 min. Under basal tension conditions laser illumination of HpD-pretreated vessels resulted in an increase in tension, whereas laser illumination of vessels not exposed to HpD did not contract. This sustained contraction was not reversed by washing the tissue with fresh Krebs-Ringer solution. Responses to norepinephrine, transmural electrical stimulation, and elevated concentrations of KCl were reduced in blood vessels tested after HpD laser illumination. Laser-induced contractions of canine carotid arteries did not require the presence of an intact vascular endothelium. Vascular effect of these photosensitizers appears to involve the formation of oxygen-derived radicals. This preparation could provide a good model for examining the effects of free radicals on vascular physiology.

scholarly journals Effects of Terpenes and Terpenoids of Natural Occurrence in Essential Oils on Vascular Smooth Muscle and on Systemic Blood Pressure: Pharmacological Studies and Perspective of Therapeutic Use

2020 ◽  
Author(s):  
Ana Carolina Cardoso-Teixeira ◽  
Klausen Oliveira-Abreu ◽  
Levy Gabriel de Freitas Brito ◽  
Andrelina Noronha Coelho-de-Souza ◽  
José Henrique Leal-Cardoso
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Biological Activities ◽  
Systemic Blood Pressure ◽  
Potential Effect ◽  
Natural Occurrence ◽  
Systemic Blood ◽  
Vascular Beds ◽  
Chemical Groups

Terpenes are a class of chemical compounds with carbon and hydrogen atoms in their structure. They can be classified into several classes according to the quantity of isoprene units present in its structure. Terpenes can have their structure modified by the addition of various chemical radicals. When these molecules are modified by the addition of atoms other than carbon and hydrogen, they become terpenoids. Terpenes and terpenoids come from the secondary metabolism of several plants. They can be found in the leaves, fruits, stem, flowers, and roots. The concentration of terpenes and terpenoids in these organs can vary according to several factors such as the season, collection method, and time of the day. Several biological activities and physiological actions are attributed to terpenes and terpenoids. Studies in the literature demonstrate that these molecules have antioxidant, anticarcinogenic, anti-inflammatory, antinociceptive, antispasmodic, and antidiabetogenic activities. Additionally, repellent and gastroprotective activity is reported. Among the most prominent activities of monoterpenes and monoterpenoids are those on the cardiovascular system. Reports on literature reveal the potential effect of monoterpenes and monoterpenoids on systemic blood pressure. Studies show that these substances have a hypotensive and bradycardic effect. In addition, the inotropic activity, both positive and negative, of these compounds has been reported. Studies also have shown that some monoterpenes and monoterpenoids also have a vasorelaxing activity on several vascular beds. These effects are attributed, in many cases to the blocking of ion channels, such as voltage-gated calcium channels. It can also be observed that monoterpenes and monoterpenoids can have their effects modulated by the action of the vascular endothelium. In addition, it has been shown that the molecular structure and the presence of chemical groups influence the potency and efficacy of these compounds on vascular beds. Here, the effect of several monoterpenes and monoterpenoids on systemic blood pressure and vascular smooth muscle will be reported.

scholarly journals An essential role of PDCD4 in vascular smooth muscle cell apoptosis and proliferation: implications for vascular disease

2010 ◽  
Vol 298 (6) ◽  
pp. C1481-C1488 ◽  
Author(s):  
Xiaojun Liu ◽  
Yunhui Cheng ◽  
Jian Yang ◽  
Thomas J. Krall ◽  
Yuqing Huo ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Carotid Arteries ◽  
Vascular Diseases ◽  
Vsmc Proliferation ◽  
Vascular Walls

It is well established that vascular smooth muscle cell (VSMC) apoptosis and proliferation are critical cellular events in a variety of human vascular diseases. However, the molecular mechanisms involved in controlling VSMC apoptosis and proliferation are still unclear. In the current study, we have found that programmed cell death 4 (PDCD4) is significantly downregulated in balloon-injured rat carotid arteries in vivo and in platelet-derived growth factor-stimulated VSMCs in vitro. Overexpression of PDCD4 via adenovirus (Ad-PDCD4) increases VSMC apoptosis in an apoptotic model induced by serum deprivation. In contrast, VSMC apoptosis is significantly decreased by knockdown of PDCD4 via its small interfering RNA. In the rat carotid arteries in vivo, VSMC apoptosis is increased by Ad-PDCD4. We have further identified that activator protein 1 is a downstream signaling molecule of PDCD4 that is associated with PDCD4-mediated effects on VSMC apoptosis. In addition, VSMC proliferation was inhibited by overexpression of PDCD4. The current study has identified, for the first time, that PDCD4 is an essential regulator of VSMC apoptosis and proliferation. The downregulation of PDCD4 expression in diseased vascular walls may be responsible for the imbalance of VSMC proliferation and apoptosis. The results indicate that PDCD4 may be a new therapeutic target in proliferative vascular diseases.

Effects of gamma radiation on isolated surviving arteries and their vasa vasorum

1961 ◽  
Vol 201 (5) ◽  
pp. 901-904 ◽  
Author(s):  
Durwood J. Smith
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Gamma Radiation ◽  
Direct Effect ◽  
Arterial Wall ◽  
Carotid Arteries ◽  
Mineral Oil ◽  
Vasa Vasorum

The effects of irradiation with Co60 on 136 swine and dog carotid arteries have been studied in vitro, utilizing an angioplethysmokymographic technique. In 20–40% of the specimens a slight vasoconstriction of the arterial wall was observed. This began and was completed within the first 60 sec of irradiation. Mounting the tissue in mineral oil did not prevent this reaction. Marked reductions in vasa vasorum flow were observed in swine carotids (70% decrease) and dog carotids (50% decrease) exposed to 9390 r of gamma radiation during 15 min. Less marked, although significant, decreases in vasa vasorum flow were seen in swine arteries exposed to 3000 r, 2085 r, and 1500 r. No significant decreases were observed in 24 arteries exposed to 843 r. Swine arteries exposed to 9390 r, while mounted in mineral oil, did not show a significant decrease in vasa vasorum flow. It is concluded that the contraction of the arterial wall was a direct effect of radiation upon the vascular smooth muscle and that the observed decrease in vasa flow was probably secondary to ionization of the Tyrode's solution surrounding the artery.

Effect of bumetanide on potassium transport and ionic composition of the arterial wall

1986 ◽  
Vol 251 (3) ◽  
pp. F537-F546 ◽  
Author(s):  
H. Cantiello ◽  
J. Copello ◽  
A. Muller ◽  
L. Mikulic ◽  
M. F. Villamil
Keyword(s):  
Smooth Muscle ◽  
Steady State ◽  
Vascular Smooth Muscle ◽  
Active Component ◽  
Arterial Wall ◽  
Carotid Arteries ◽  
Inhibitory Concentration ◽  
Ionic Composition ◽  
Potassium Transport

Bumetanide (B) (1 mM) decreased K content of dog carotid arteries (Ka) by 11-15%, K turnover (lambda 2) by 31%, and steady-state K fluxes (JK) by approximately 48%. The drug also reduced intracellular (ic) Cl, H2O, and occasionally ic Na. The half-maximal inhibitory concentration of B on JK was close to 40 microM. However, 10 microM still fully reduced ic K, Cl, and H2O but not ic Na. Replacement of external Cl by sulfate or nitrate mimicked the B effects on JK and reduced its capacity of inhibition by approximately 40 and approximately 80%, respectively. Replacement of Na by choline decreased Ka and JK by 90 and 96%, respectively, and rendered B totally ineffective. B also decreased Cl uptake and content of cultured vascular smooth muscle and ic Cl and H2O of whole arteries. Ouabain (Ou) (1 mM) decreased Ka 90%, accelerated lambda 2 four- to fivefold, and reduced JK 45%. Addition of B or removal of external Na or Cl in the presence of Ou returned lambda 2 to normal levels and reduced the residual JK by approximately 90% but failed to further decrease the Ka. According to these data, B mainly inhibits a coupled KCl passive self exchange plus a smaller active net KCl influx. Ou abolished the active component without affecting the passive self exchange. The presence of Na is necessary for the operation of the KCl-coupled self exchange, and Na gradients may provide the energy for the uphill KCl movements.

Expression of granulocyte colony-stimulating factor is induced in injured rat carotid arteries and mediates vascular smooth muscle cell migration

2005 ◽  
Vol 288 (1) ◽  
pp. C81-C88 ◽  
Author(s):  
Xing Chen ◽  
Sheri E. Kelemen ◽  
Michael V. Autieri
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Balloon Angioplasty ◽  
Carotid Arteries ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Important Mediator ◽  
Stimulating Factor

Granulocyte colony-stimulating factor (G-CSF) is a lineage-restricted hematopoietic growth factor that stimulates proliferation and maturation of hematopoietic progenitors and is a known powerful mobilizer of bone marrow-derived stem cells. Very little has been reported on G-CSF expression and modulation of vascular smooth muscle cell (VSMC) activation. The purpose of this study was to characterize the expression and effects of G-CSF on primary human VSMC and balloon angioplasty-injured rat carotid arteries. In cultured human VSMC, G-CSF mRNA and protein expression are induced by several cytokines, with the most potent being fetal calf serum and T-lymphocyte-conditioned media. G-CSF is not expressed in naive rat carotid arteries but is induced in neointimal SMC in carotid arteries subject to balloon angioplasty. G-CSF is chemotactic for human VSMC. There is a significant difference between unstimulated cells and those treated with G-CSF at 100 and 1,000 pg/ml ( P < 0.01 and 0.05 for 3 experiments). G-CSF also activates the GTPase Rac1, a regulator of cellular migration in VSMC. Inhibition of Rac1 inhibits G-CSF-driven VSMC migration. Important signal transduction protein kinases, including p44/42 MAPK, Akt, and S6 kinase, are also activated in response to G-CSF. This is the first report describing the expression of G-CSF in injured arteries and the multiple effects of G-CSF on VSMC activation. Together, our data suggest that G-CSF is an important mediator of inflammatory cell-VSMC communication and VSMC autocrine activation and may be an important mediator of the VSMC response to injury.

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