scholarly journals Effect ofCymbopogon citratusand Citral on Vascular Smooth Muscle of the Isolated Thoracic Rat Aorta

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
R. Chitra Devi ◽  
S. M. Sim ◽  
R. Ismail
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Relaxation Effect ◽  
Rat Aorta ◽  
Major Constituent ◽  
Protective Properties ◽  
Relaxant Effect ◽  
Vasorelaxant Effect ◽  
Methanolic Extracts ◽  
Dose Dependent

Cymbopogon citratushas been shown to have antioxidant, antimicrobial, antispasmodic and chemo-protective properties. Citral, is the major constituent ofC. citratus. This study investigated the effects of methanolic extracts of leaves (LE), stems (SE), and roots (RE) ofC. citratusand citral on vascular smooth muscle and explored their possible mechanisms of action. The experiment was conducted using isolated tissue preparations, where citral, LE, SE, and RE were added separately into a tissue bath that contained aortic rings, which were pre-contracted with phenylephrine (PE). Citral, LE, and RE exhibited a dose-dependent relaxant effect on the PE-induced contractions. Citral appeared to partially act via NO as its vasorelaxant effect was attenuated by L-NAME. However, the effect of LE may involve prostacyclin as indomethacin reversed the relaxant effect of LE on the PE-induced contraction. Furthermore, citral, LE, and RE abolished the restoration of PE-induced contraction caused by the addition of increasing doses of calcium in both endothelium intact and denuded rings. These findings suggest that the relaxation effect of citral, LE, and RE is endothelium-independent and may be mainly by affecting the intracellular concentration of calcium. Citral may partially act through the NO pathway while a vasodilator prostaglandin may mediate the effect of LE.

scholarly journals The Vasorelaxant Effect ofp-Cymene in Rat Aorta Involves Potassium Channels

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Martapolyana T. M. Silva ◽  
Fernanda P. R. A. Ribeiro ◽  
Maria Alice M. B. Medeiros ◽  
Pedrita A. Sampaio ◽  
Yonara M. S. Silva ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Potassium Channels ◽  
Vascular Smooth Muscle ◽  
Channel Blocker ◽  
Antimicrobial Activities ◽  
Rat Aorta ◽  
Relaxant Effect ◽  
Vasorelaxant Effect ◽  
Dose Dependent ◽  
Relaxing Effect

The monoterpenes are the main constituents of most essential oils andp-cymene is a monoterpene commonly found in various species of aromatic herbs, which has been reported for anti-inflammatory, antinociceptive, and antimicrobial activities. However, there is no report concerning its pharmacological activity on the vascular smooth muscle. The aim of current work was to investigate the effects ofp-cymene in isolated rat aorta and also study its mechanism of action. In this work, we show thatp-cymene has a relaxant effect, in a dose-dependent way, on the vascular smooth muscle, regardless of the presence of the endothelium. Using a nonselective potassium channel blocker, the CsCl, the relaxant effect ofp-cymene was attenuated. In the presence of more selective potassium channels blockers, such as TEA or 4-AP, no change in the relaxant effect ofp-cymene was evidenced, indicating thatBKCaandKVchannels are not involved in that relaxant effect. However, in the presence of glibenclamide or BaCl2,KATPandKirblockers, respectively, the relaxant effect ofp-cymene was attenuated. The data presented indicate thatp-cymene has a relaxing effect on rat aorta, regardless of the endothelium, but with the participation of theKATPandKirchannels.

Nickel inhibits endothelin-induced contractions of vascular smooth muscle

1990 ◽  
Vol 258 (6) ◽  
pp. C1025-C1030 ◽  
Author(s):  
K. Blackburn ◽  
R. F. Highsmith
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Isometric Force ◽  
Inhibitory Effect ◽  
Rat Aorta ◽  
Porcine Coronary Artery ◽  
Force Development ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Dose Dependent

Endothelin (ET)-induced contractions of vascular smooth muscle (VSM) are dependent on extracellular Ca2+ yet display only partial sensitivity to L-type Ca2+ antagonists. The purpose of this study was to evaluate the effect of nickel (Ni2+), a Ca2+ channel antagonist with clearly documented differential potency toward L- vs. T-type Ca2+ currents on ET-mediated contractions in VSM. Treatment of rings of left anterior descending porcine coronary artery (LAD) with Ni2+ produced a profound dose-dependent inhibition of isometric force development in response to porcine ET (ET-1). At a concentration of 360 microM, Ni2+ exerted a significant inhibitory effect on contracture in response to doses of ET-1 ranging from 3 to 100 nM. In contrast, the same concentration of Ni2+ failed to significantly affect peak force development in response to KCl depolarization (5-77 mM) or to phenylephrine (0.3-30 mM). In addition, 360 microM Ni2+ significantly inhibited the contractile response of rat aorta to 10 nM ET-1. We conclude that ET-1 activates a Ni2(+)-sensitive process in VSM which may signal an additional Ca2+ influx pathway that appears to be functionally distinct from the L-type Ca2+ channel.

scholarly journals EVALUATION OF IN-VITRO VASORELAXANT EFFECT (POTENTIAL ANTIHYPERTENSIVE) OF KIGELIA AFRICANA FRUIT METHANOL EXTRACT ON POTASSIUM CHLORIDE AND PHENYLEPHRINE INDUCED TENSION IN WISTAR RAT AORTA

2020 ◽  
Vol 4 (3) ◽  
pp. 470-475
Author(s):  
A. O. Isah ◽  
M. Idu ◽  
A. A. Abdulrahman ◽  
F. Amaechina
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Potassium Chloride ◽  
Methanol Extract ◽  
Muscle Relaxation ◽  
Rat Aorta ◽  
Smooth Muscle Relaxation ◽  
Organ Bath ◽  
Vasorelaxant Effect

This research on Kigelia africana was conducted in order to ascertain its ability to relax excited vascular smooth muscle in rat aorta. Preliminary investigation on whether the plant exhibits antihypertensive property was done before the evaluation of in vitro vasorelaxant effect. The vasorelaxant activity was determined using in vitro method on rat aorta with the aid of perfusion apparatus with a detachable organ bath. The administration of potassium chloride (KCl) raised the tension from 1.0 to 1.31 indicating that the aorta got to its peak of contraction. At 10 and 20mg/kg, the tension dropped significantly, showing relaxation of the smooth muscle while at 5mg/kg, drop in tension was insignificant at p˂0.05. However, at some of the doses, towards the end of experiment, there was steady resurge in tension showing that the aorta resumed contraction. On the application of phenylephrine (PE), the tension rose to 1.18g. On administration of the extract, the tension dropped slightly showing mild vascular smooth muscle relaxation. From the results obtained, there was seeming similarity in the action of the K. africana compared to amlodipine/Ramipril in KCl and PE induced tension in aorta respectively. However, at 10 and 20mg/kg, a substantial decrease in tension was noted indicating that the extract action is dose dependent. Thus, from this in-vitro smooth muscle relaxation study in rats, the methanol extract of K. africana has depressant property that was likely expressed by enhancing the closing of voltage operated calcium channel and ACE inhibiting activity in KCl and Phenylephrine induced tension respectively.

Impact of α1-adrenoceptor expression on contractile properties of vascular smooth muscle cells

2007 ◽  
Vol 293 (3) ◽  
pp. R1215-R1221 ◽  
Author(s):  
Adrian Gericke ◽  
Peter Martinka ◽  
Irina Nazarenko ◽  
Pontus B. Persson ◽  
Andreas Patzak
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Low Frequency ◽  
Rat Aorta ◽  
Contractile Properties ◽  
Isolated Cells ◽  
Functional Studies ◽  
Sympathetic Modulation ◽  
Dose Dependent ◽  
Subtype Distribution

Low-frequency blood pressure oscillations (Mayer waves) are discussed as a marker for sympathetic modulation of vascular tone. However, the factors that determine the frequency response of the vasculature to sympathetic stimuli are not fully understood. Possible mechanisms include functions related to α1-adrenergic receptors (α1-AR) and postreceptor processes involved in the vascular contractile response. The purpose of the present study was to examine the hypothesis that expression levels of α1-AR and their subtype distribution determine velocity and magnitude of α1-AR-mediated vascular smooth muscle cell (VSMC) contraction. α1A-, α1B-, and α1D-AR subtypes were transfected into VSMCs from rat aorta and characterized immunocytochemically via confocal microscopy. Functional studies in isolated cells were performed using video microscopy. The α1-AR agonist phenylephrine produced dose-dependent contractions of VSMCs. All transfected groups were more sensitive to phenylephrine compared with controls. Maximal contraction velocity almost doubled in transfected cells. However, no differences in observed parameters were found between the three transfected groups. Contractile properties in response to membrane depolarization with KCl were similar in all groups. In conclusion, α1-AR density determines velocity and sensitivity of α1-AR-mediated contraction in VSMCs. α1-AR subtype distribution does not appear to influence vasoconstriction to sympathetic stimuli.

Epidermal growth factor-mediated effects on equine vascular smooth muscle cells

1988 ◽  
Vol 255 (4) ◽  
pp. C447-C451 ◽  
Author(s):  
D. A. Grosenbaugh ◽  
M. S. Amoss ◽  
D. M. Hood ◽  
S. J. Morgan ◽  
J. D. Williams
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Dna Synthesis ◽  
Vascular Smooth Muscle Cells ◽  
Cellular Proliferation ◽  
Epidermal Growth ◽  
Dose Dependent

Epidermal growth factor (EGF) receptor binding kinetics and EGF-mediated stimulation of DNA synthesis and cellular proliferation were studied in cultured vascular smooth muscle cells (VSMC) from the equine thoracic aorta. Binding studies, using murine 125I-labeled EGF, indicate the presence of a single class of high-affinity binding sites (apparent KD = 2.8 X 10(-11) M), with an estimated maximal binding capacity of 5,800 sites/cell. EGF stimulated [3H]thymidine uptake in confluent quiescent monolayers in a dose-dependent fashion, half-maximal stimulation occurring at 7.5 X 10(-11) M. Likewise, EGF-mediated cellular proliferation was dose dependent (50% effective dose = 5 X 10(-11) M) under reduced serum concentrations. Equine VSMC contain specific receptors for EGF, and EGF can stimulate DNA synthesis and proliferation in these cultured cells, which suggests that EGF may participate in the proliferative changes observed in equine distal digital peripheral vascular disease.

scholarly journals Cell–Cell Interaction of Macrophages and Vascular Smooth Muscle Cells in the Synthesis of Leukotriene B4

1994 ◽  
Vol 3 (4) ◽  
pp. 297-302 ◽  
Author(s):  
M. Zou ◽  
C. Anges
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Cell Interaction ◽  
Leukotriene B4 ◽  
Factor Α ◽  
Dose Dependent ◽  
Cell Cell

Biosynthesis of LTB4during cell-cell interaction between vascular smooth muscle cells (SMC) and alveolar macrophages (AM) has been investigated by use of both high-pressure Hquid chromatography (HPLC) and radtoimmunoassay (RIA). Both interleukin-β (IL-β) and tumour necrosis factor-α (TNFα) induced a time- and dose-dependent synthesis of 15-, and 5-hydroxyeicosatetraenoic acids (HETEs) from cultured SMC. However, neither TNFα nor IL-1β induced a significant LTB4production in SMC alone or AM alone after 24 h of incubation. Addition of IL-1β and TNFα simultaneously to SMC resulted in a dose-dependent synergistic increase of HETEs. Macrophages dose-dependently transformed extremely low concentrations of exogenous LTA4into LTB4. Incubation of vascular SMC with various numbers of AM in the presence of IL-1β (5 units/ml) and TNFα (10 units/ml) induced a great increase of LTB4synthesis in comparison with the detectable levels of LTB4produced by macrophages alone. Pretreatment of SMC with NDGA, cycloheximide, and actinomycin not only inhibited IL-1 and TNT induced HETEs synthesis but also abolished LTB4production when co-incubated with macrophages. These results suggest that LTB4in a mixture of SMC and macrophages could originate from a transcellular metabolism, i.e. macrophages transforming SMC-derived LTA4into LTB4.

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