scholarly journals Sulfur dioxide relaxes rat aorta by endothelium-dependent and -independent mechanisms

2009 ◽  
pp. 521-527 ◽  
Author(s):  
Y-K Wang ◽  
A-J Ren ◽  
X-Q Yang ◽  
L-G Wang ◽  
W-F Rong ◽  
...  
Keyword(s):  
Sulfur Dioxide ◽  
Thoracic Aorta ◽  
Vascular Tissue ◽  
Rat Aorta ◽  
Isometric Tension ◽  
Organ Bath ◽  
Kca Channels ◽  
Voltage Dependent ◽  
Rat Thoracic Aorta ◽  
High Doses

This study aimed to investigate the vasoactivity of sulfur dioxide (SO2), a novel gas identified from vascular tissue, in rat thoracic aorta. The thoracic aorta was isolated, cut into rings, and mounted in organ-bath chambers. After equilibrium, the rings were gradually stretched to a resting tension. Isometric tension was recorded under the treatments with vasoconstrictors, SO2 derivatives, and various drugs as pharmacological interventions. In endothelium-intact aortic rings constricted by 1 μM phenylephrine (PE), SO2 derivatives (0.5 – 8 mM) caused a dosedependent relaxation. Endothelium removal and a NOS inhibitor L-NAME reduced the relaxation to low doses of SO2 derivatives, but not that to relatively high doses (≥ 2 mM). In endotheliumdenuded rings, SO2 derivatives attenuated vasoconstriction induced by high K+ (60 mM) or CaCl2 (0.01-10 mM). The relaxation to SO2 derivatives in PE-constricted rings without endothelium was significantly inhibited by blockers of ATPsensitive K+ (KATP) and Ca2+-activated K+ (KCa) channels, but not by those of voltage-dependent K+ channels, Na+-K+-ATPase or Na+-Ca2+ exchanger. SO2 relaxed vessel tone via endotheliumdependent mechanisms associated with NOS activation, and via endothelium-independent mechanisms dependent on the inhibition of voltage-gated Ca2+ channels, and the opening of KATP and KCa channels.

Testosterone-induced relaxation of rat aorta is androgen structure specific and involves K+ channel activation

2001 ◽  
Vol 91 (6) ◽  
pp. 2742-2750 ◽  
Author(s):  
Andrew Q. Ding ◽  
John N. Stallone
Keyword(s):  
Rank Order ◽  
Specific Effect ◽  
Rat Aorta ◽  
Isometric Tension ◽  
K Channel ◽  
Delayed Rectifier ◽  
Sprague Dawley ◽  
Voltage Dependent ◽  
Rat Thoracic Aorta ◽  
Lower Permeability

Recent studies have established that testosterone (Tes) produces acute (nongenomic) vasorelaxation. This study examined the structural specificity of Tes-induced vasorelaxation and the role of vascular smooth muscle (VSM) K+ channels in rat thoracic aorta. Aortic rings from male Sprague-Dawley rats with (Endo+) and without endothelium (Endo−) were prepared for isometric tension recording. In Endo− aortas precontracted with phenylephrine, 5–300 μM Tes produced dose-dependent relaxation from 10 μM (4 ± 1%) to 300 μM (100 ± 1%). In paired Endo+ and Endo− aortas, Tes-induced vasorelaxation was slightly but significantly greater in Endo+ aortas (at 5–150 μM Tes); sensitivity (EC50) of the aorta to Tes was reduced by nearly one-half in Endo− vessels. Based on the sensitivity (EC50) of Endo− aortas, Tes, the active metabolite 5α-dihydrotestosterone, the major excretory metabolites androsterone and etiocholanolone, the nonpolar esters Tes-enanthate and Tes-hemisuccinate (THS), and THS conjugates to BSA (THS-BSA) exhibited relative potencies for vasorelaxation dramatically different from androgen receptor-mediated effects observed in reproductive tissues, with a rank order of THS-BSA > Tes > androsterone = THS = etiocholanolone > dihydrotestosterone ≫ Tes-enanthate. Pretreatment of aortas with 5 mM 4-aminopyridine attenuated Tes-induced vasorelaxation by an average of 44 ± 2% (25–300 μM Tes). In contrast, pretreatment of aortas with other K+ channel inhibitors had no effect. These data reveal that Tes-induced vasorelaxation is a structurally specific effect of the androgen molecule, which is enhanced in more polar analogs that have a lower permeability to the VSM cell membrane, and that the effect of Tes involves activation of K+ efflux through K+channels in VSM, perhaps via the voltage-dependent (delayed-rectifier) K+ channel.

scholarly journals Cilostazol enhances atorvastatin-induced vasodilation of female rat aorta during aging

2017 ◽  
Vol 104 (3) ◽  
pp. 226-234 ◽  
Author(s):  
KE Nurullahoğlu-Atalık ◽  
S Kutlu ◽  
H Solak ◽  
R Özen Koca
Keyword(s):  
Thoracic Aorta ◽  
Inhibitory Effect ◽  
Rat Aorta ◽  
Organ Bath ◽  
Female Rat ◽  
Response Curves ◽  
Adult Rat ◽  
Combined Application ◽  
Female Wistar Rats ◽  
Rat Thoracic Aorta

Statins have cholesterol-independent effects including an increased vascular nitric oxide activity and are commonly used by patients with cardiovascular disease. Such patients frequently have cardiovascular diseases, which may be treated with cilostazol, a platelet aggregation inhibitor. This study was designed to investigate whether combined use of cilostazol would increase the inhibitory effect of statin on vascular smooth muscle and how maturation would affect these responses. Female Wistar rats, aged 3–4 months (young) and 14–15 months (adult), were sacrificed by cervical dislocation and the thoracic aorta was dissected and cut into 3- to 4-mm-long rings. The rings were mounted under a resting tension of 1 g in a 20-ml organ bath filled with Krebs–Henseleit solution. Rings were precontracted with phenylephrine (10−6 M), and the presence of endothelium was confirmed with acetylcholine (10−6 M). Then, the concentration–response curves were obtained for atorvastatin alone (10−10 to 3 × 10−4 M; control) and in the presence of cilostazol (10−6 M) in young and adult rat aortas. This experimental protocol was also carried out in aorta rings, which had been pretreated with NG-nitro-l-arginine methyl ester (l-NAME, 10−4 M). Atorvastatin induced concentration-dependent relaxations in young and adult rat thoracic aorta rings precontracted with phenylephrine. The pIC50 value of atorvastatin was significantly decreased in adult rat aortas. In addition, pretreatment of aortas with cilostazol enhanced the potency of atorvastatin in both young and adult aortas. Incubation with l-NAME did not completely eliminate the relaxations to atorvastatin in the presence of cilostazol. These results suggest that combined application of cilostazol with atorvastatin was significantly more potent than atorvastatin alone. Combined drug therapy may be efficacious in delaying the occurrence of cardiovascular events.

scholarly journals Comparative Contractile Effects of Halothane and Sevoflurane in Rat Aorta

2000 ◽  
Vol 92 (1) ◽  
pp. 219-219 ◽  
Author(s):  
Vu Huu Vinh ◽  
Taijiro Enoki ◽  
Shinichi Hirata ◽  
Hiroshi Toda ◽  
Masahiro Kakuyama ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Thoracic Aorta ◽  
Volatile Anesthetic ◽  
Rat Aorta ◽  
Isometric Tension ◽  
Dependent Manner ◽  
Anesthetic Agents ◽  
Rat Thoracic Aorta ◽  
Dose Dependent ◽  
Ca2 Channels

Background Volatile anesthetic agents have been shown to have contractile effects in vascular tissues during specific conditions. This study compared contractile effects of halothane and sevoflurane in rat aorta treated with verapamil. This study also tried to elucidate the mechanism of the contraction. Methods Endothelium-denuded rat thoracic aorta was used for recording of isometric tension and measurement of influx of 45Ca2+. All experiments were performed in the presence of verapamil. In recording of tension, rings were precontracted with a submaximum dose of phenylephrine, followed by exposure to halothane or sevoflurane. For measurement of influx of 45Ca2+, rat aortic strips were exposed to phenylephrine and then to additional halothane or sevoflurane. Influx of Ca2+ was estimated by incubating the strips in 45Ca2+-labeled solution for 2 min. Results Halothane (0.5-4.0%) induced contraction in a dose-dependent manner, whereas sevoflurane (1-4%) had no effect on tension. Influx of 45Ca2+ was strongly enhanced by halothane at 1% and 2%, but only slightly at 4%, and was not affected by 1-4% sevoflurane. SK&F 96365, a blocker of voltage-independent Ca2+ channels, abolished contraction and influx of 45Ca2+ by 1% halothane. Depletion of Ca2+ from the sarcoplasmic reticulum with ryanodine or thapsigargin reduced the contraction induced by halothane at 4% but not that at 1% and 2%. Conclusion Halothane is suggested to cause contraction by enhancing influx of Ca2+ via voltage-independent Ca2+ channels at concentrations up to 2% and by inducing release of Ca2+ at 4%. Sevoflurane (1-4%) is devoid of these contractile effects.

Effects of forskolin and cyclic nucleotides on isometric force in rat aorta

1986 ◽  
Vol 250 (3) ◽  
pp. C468-C473 ◽  
Author(s):  
E. G. McMahon ◽  
R. J. Paul
Keyword(s):  
Cyclic Nucleotides ◽  
Cyclic Nucleotide ◽  
Isometric Force ◽  
Rat Aorta ◽  
Isometric Tension ◽  
Tension Development ◽  
Nucleotide Analogues ◽  
Cyclic Monophosphate ◽  
Contractile System ◽  
Rat Thoracic Aorta

The present study was undertaken to determine the extent to which cyclic nucleotide-induced relaxation in the intact rat aorta is mediated at the level of the contractile system. The relaxant effects of the cyclic nucleotide analogues [8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP) and dibutyryladenosine 3',5'-cyclic monophosphate (DBcAMP)] and forskolin were examined in both the intact vessel and a Triton X-100-skinned preparation of rat thoracic aorta. Relaxation of a norepinephrine-induced contraction was essentially complete 30 min after the addition of 50 microM 8-BrcGMP [% relaxation = 87.2 +/- 4.4% (n = 4)], 100 microM DBcAMP [98.2 +/- 1.2% (n = 4)], and 1 microM forskolin [107.0 +/- 3.3% (n = 5)]. These same doses were ineffective in relaxing precontracted skinned rat aortic rings compared with the relaxation achieved in the intact vessel. The largest relaxation in the skinned aortas was achieved with the addition of 1 microM forskolin [17.4 +/- 1.5% (n = 4)]. The addition of catalytic subunit of cAMP-dependent protein kinase had no effect on isometric tension in the precontracted skinned aorta. Preincubation with the cyclic nucleotide analogues or forskolin in a low-Ca2+ solution (pCa less than 8) was also ineffective in inhibiting subsequent isometric tension development. Our results suggest that only a very small fraction of the relaxation with cyclic nucleotides and forskolin in the intact rat aorta is due to the action of these agents at the level of the contractile system.

Androgen-receptor defect abolishes sex differences in nitric oxide and reactivity to vasopressin in rat aorta

2001 ◽  
Vol 91 (6) ◽  
pp. 2602-2610 ◽  
Author(s):  
John N. Stallone ◽  
Ronald L. Salisbury ◽  
Clifford T. Fulton
Keyword(s):  
Nitric Oxide ◽  
Androgen Receptor ◽  
Methyl Ester ◽  
Thoracic Aorta ◽  
Vascular Reactivity ◽  
Rat Aorta ◽  
Maximal Response ◽  
Maximal Contraction ◽  
Rat Thoracic Aorta ◽  
Recessive Defect

Contractions of rat thoracic aorta to vasopressin (VP) are threefold higher in females (F) than in males (M), primarily because nitric oxide (NO) attenuation of contraction is greater in M. To determine the role of the androgen receptor (AR) in this mechanism, vascular reactivity to VP was examined in thoracic aorta of the testicular-feminized male (Tfm) rat, which has an X-linked, recessive defect in AR function in affected M. Maximal contraction of normal aortas to VP was fourfold higher in F (4,128 ± 291 mg/mg ring wt) than in M (971 ± 133 mg); maximal response of Tfm (3,967 ± 253 mg) was similar to that of normal F. N G-nitro-l-arginine methyl ester increased maximal response to VP threefold in M but had no effect in F or Tfm. In contrast, maximal contraction of normal aortas to phenylephrine was 43% higher in M (4,011 ± 179 mg) than in F (2,809 ± 78 mg); maximal response of Tfm (2,716 ± 126 mg) was similar to that of normal F. N G-nitro-l-arginine methyl ester increased maximal response to phenylephrine by >50% in F and Tfm but had no effect in M. Maximal contractile response to 80 mM KCl did not differ among M, F, or Tfm. Thus androgens and normal vascular AR function are important in the greater NO-mediated attenuation of reactivity to VP in M than in F rat aorta, which may involve specific modulation of endothelial VP signal transduction pathways and NO release by androgens. These data also establish the importance of the Tfm rat as a model to study the effects of androgens on cardiovascular function.

Rivaroxaban-Mediated Vascular Relaxation As a Potential Cause of Headaches and Dizziness

Blood ◽  
2015 ◽  
Vol 126 (23) ◽  
pp. 2334-2334
Author(s):  
Jon Mabley ◽  
Greg Scutt ◽  
Kathryn Jane Lang ◽  
Jignesh P Patel ◽  
Roopen Arya
Keyword(s):  
Thoracic Aorta ◽  
Research Funding ◽  
Adult Population ◽  
Underlying Mechanism ◽  
Physiological Effect ◽  
Isometric Tension ◽  
Common Side Effect ◽  
Sprague Dawley ◽  
Relaxant Effect ◽  
Rat Thoracic Aorta

Abstract The availability of the direct Xa inhibitors apixaban, edoxaban and rivaroxaban in clinical practice is leading a paradigm shift in anticoagulation for the management of venous thromboembolism (VTE) and stroke prophylaxis in the context of non-valvular atrial fibrillation (AF). A common side effect experienced by patients receiving rivaroxaban in clinical trials was dizziness and headache, with a reported incidence of between 1 in 10 and 1 in 100 patients. Clinical experience has seen patients reporting rivaroxaban associated headaches and dizziness, leading to discontinuation of therapy. Given that widespread use of these agents is likely to be within an older adult population, it is important to understand the mechanism behind clinical observations which may then allow us to determine why some patients are affected more than others. We hypothesise that rivaroxaban directly causes vascular arteriodilation, resulting in headaches and dizziness requiring discontinuation of treatment. To test this hypothesis the effects of rivaroxaban on phenylephrine pre-contracted rat aortic rings was investigated. Thoracic aorta from male Sprague-Dawley rats (180-220g) were dissected and cut into rings of 2-3mm prior to being mounted under a preload tension of 1.5g in Krebs filled organ baths. Isometric tension of the rings was measured with isometric transducers (Danish Myo Technology, Aarhus, Denmark) digitised using a Power lab system. Following a phenylephrine dose-response curve the aortic rings were pre-contracted with 1 µM phenylephrine before measuring the relaxant effect of rivaroxaban (0.001-0.3 µM) or a similar volume of the vehicle dimethyl sulfoxide (DMSO). Statistical analysis was carried out using two-way ANOVA with Bonferroni's correction, where p<0.05 was considered significant. Exposure of aortic rings to both rivaroxaban and the vehicle DMSO caused relaxation. However, the relaxation observed with rivaroxaban was significantly greater than that observed with the vehicle (Fig 1). Our preliminary data suggests that rivaroxaban may have a direct arteriodilatory effect. This arteriodilatory effect of rivaroxaban may provide a possible explanation for dizziness and headaches experienced by some rivaroxaban treated patients. Further work is required to determine the underlying mechanism of rivaroxaban-mediated vaso-relaxant effect as well as determining if the other Xa inhibitors apixaban and edoxaban also share this physiological effect, and if so, to what extent. Figure 1. Exposure of rat thoracic aorta rings to rivaroxaban and the vehicle DMSO caused relaxation. Rivaroxaban produced significantly more relaxation as compared to DMSO alone (p<0.05). Data is expressed as mean ± SEM from 12 animals; †p<0.05 vs. DMSO alone Figure 1. Exposure of rat thoracic aorta rings to rivaroxaban and the vehicle DMSO caused relaxation. Rivaroxaban produced significantly more relaxation as compared to DMSO alone (p<0.05). Data is expressed as mean ± SEM from 12 animals; †p<0.05 vs. DMSO alone Disclosures Patel: Bayer plc: Research Funding. Arya:Bayer plc: Research Funding.

scholarly journals Irisin relaxes rat thoracic aorta: MEK1/2 signaling pathway, KV channels, SKCa channels, and BKCa channels are involved in irisin-induced vasodilation

2021 ◽  
Author(s):  
Sadettin Demirel ◽  
Serdar Sahinturk ◽  
Naciye Isbil ◽  
Fadil Ozyener
Keyword(s):  
Thoracic Aorta ◽  
Channel Blocker ◽  
Mitogen Activated Protein Kinase ◽  
Control Group ◽  
Organ Bath ◽  
Dependent Manner ◽  
Bkca Channels ◽  
Kv Channels ◽  
Rat Thoracic Aorta ◽  
Relaxation Responses

In this study, it was aimed to investigate the effects of irisin on vascular smooth muscle contractility in rat thoracic aorta, and the hypothesis that mitogen-activated protein kinase kinase (MEK1/2) signalling pathway, voltage-gated potassium (KV) channels, small-conductance calcium-activated potassium (SKCa) channels, and large-conductance calcium-activated potassium (BKCa) channels may have roles in these effects. Isometric contraction-relaxation responses of isolated thoracic aorta rings were measured with an organ bath model. The steady contraction was induced with 10-5 M phenylephrine (PHE), and then the concentration-dependent responses of irisin (10-9-10-6 M) were examined. Irisin exerted the vasorelaxant effects at concentrations of 10-8, 10-7, and 10-6 M compared to the control group (p<0.001). Besides, MEK1/2 inhibitor U0126, KV channel blocker XE-991, SKCa channel blocker apamin, and BKCa channel blocker tetraethylammonium (TEA) incubations significantly inhibited the irisin-induced relaxation responses. In conclusion, the first physiological findings were obtained regarding the functional relaxing effects of irisin in rat thoracic aorta. The findings demonstrated that irisin induces relaxation responses in endothelium-intact aortic rings in a concentration-dependent manner. Furthermore, this study is the first to report that irisin-induced relaxation responses are related to the activity of the MEK1/2 pathway, KV channels, and calcium-activated K+ (SKCa and BKCa) channels.

Role of endothelium in sexual dimorphism in vasopressin-induced contraction of rat aorta

1993 ◽  
Vol 265 (6) ◽  
pp. H2073-H2080 ◽  
Author(s):  
J. N. Stallone
Keyword(s):  
Contractile Response ◽  
Rat Aorta ◽  
Isometric Tension ◽  
No Synthase ◽  
Maximal Response ◽  
Sprague Dawley ◽  
Phenylephrine Hydrochloride ◽  
Rat Thoracic Aorta ◽  
Increased Sensitivity

In rat thoracic aorta, contractile responses to arginine vasopressin (AVP) are twofold higher in females than in males. To determine the role of the endothelium in this phenomenon, the effects of endothelium removal and inhibition of nitric oxide (NO) synthase and cyclooxygenase were examined in thoracic aortas prepared from male and female Sprague-Dawley rats and mounted for isometric tension recording. Maximal contractile response to AVP was substantially higher in female (4,232 +/- 316 mg/mg ring dry wt) than in male aortas (1,365 +/- 239; P < 0.01). Removal of the endothelium markedly potentiated maximal response to AVP in male aortas (4,100 +/- 422 mg/mg ring wt; P < 0.01); endothelium removal increased sensitivity but not maximal response in female aortas. Inhibition of NO synthase with NG-monomethyl-L-arginine (L-NMMA, 250 microM) doubled maximal contraction to AVP in male aortas (3,175 +/- 193 mg/mg ring wt; P < 0.01); L-NMMA increased sensitivity but not maximal response in female aortas. Inhibition of cyclooxygenase with indomethacin (10 microM) did not alter maximal response to AVP in male aortas but significantly attenuated responses of female aortas (2,816 +/- 306 mg/mg ring wt; P < 0.01). In contrast, maximal contractile response to phenylephrine hydrochloride (PE) was 40% higher in males than in females (P < 0.01); L-NMMA increased both the sensitivity and maximal response to PE to a greater extent in female (3,061 +/- 121 vs. 4,971 +/- 135 mg/mg ring wt; P < 0.01) than in male aortas (4,317 +/- 227 vs. 4,899 +/- 104 mg/mg ring wt; P < 0.01). (ABSTRACT TRUNCATED AT 250 WORDS)

Regulation of β-adrenoceptor-mediated relaxation of the rat aorta is modulated by endogenous ovarian hormones

2000 ◽  
Vol 98 (4) ◽  
pp. 381-387 ◽  
Author(s):  
María V. CONDE ◽  
Jesús MARÍN ◽  
Carmen FERNÁNDEZ-CRIADO ◽  
NGloria BALFAGÓ
Keyword(s):  
Thoracic Aorta ◽  
Ovarian Hormones ◽  
Rat Aorta ◽  
Nitric Oxide Donor ◽  
Ovx Rats ◽  
Adrenoceptor Agonist ◽  
Stimulatory G Protein ◽  
Female Wistar Rats ◽  
Rat Thoracic Aorta ◽  
Adrenoceptor Agonists

The aim of this study was to assess the influence of the endogenous status of ovarian hormones on the relaxation induced by the β-adrenoceptor agonists isoprenaline (isoproterenol) and dobutamine in thoracic aorta segments, precontracted with noradrenaline, from age-matched (13-week-old) virgin (oestrus) and ovariectomized (OVX) prepubertal female Wistar rats. Isoprenaline-induced relaxation was decreased in intact aortic segments from OVX rats compared with that in segments from oestrus rats. Relaxation was significantly reduced by endothelium removal, 1 µmol/l propranolol or 100 µmol/l NG-nitro-l-arginine methyl ester (l-NAME). The β1-adrenoceptor agonist dobutamine induced less relaxation in intact arteries from oestrus rats than did isoprenaline, and dobutamine-induced relaxation was markedly less in intact segments from OVX compared with oestrus rats. This dobutamine-induced relaxation was abolished by endothelium removal, and reduced by 1 µmol/l propranolol, 100 µmol/l l-NAME or 1 µmol/l yohimbine. Cholera toxin (an activator of the stimulatory G-protein Gs) caused relaxation in intact arteries from oestrus rats; this relaxation was decreased by both deprivation of ovarian hormones and endothelium removal. Forskolin (a direct activator of the catalytic subunit of adenylate cyclase) and sodium nitroprusside (a nitric oxide donor and cGMP-dependent vasodilator agonist) induced similar endothelium-independent relaxation in arteries from both oestrus and OVX rats. These results suggest that the relaxation elicited by endothelial β-adrenoceptor activation in the rat thoracic aorta is impaired by deprivation of female ovarian hormones; this impairment is caused, at least in part, by decreases in both the endothelial release of NO and Gs function.

scholarly journals Long-lasting endothelium-dependent relaxation of isolated arteries caused by an extract from the bark of Combretum leprosum

2015 ◽  
Vol 13 (3) ◽  
pp. 395-403 ◽  
Author(s):  
Francisco das Chagas Alves Filho ◽  
Paulo Marques da Silva Cavalcanti ◽  
Rita de Cassia Aleixo Tostes Passaglia ◽  
Gustavo Ballejo
Keyword(s):  
Thoracic Aorta ◽  
Ruthenium Red ◽  
Organ Bath ◽  
Period 2 ◽  
Combretum Leprosum ◽  
Rat Thoracic Aorta ◽  
Isolated Arteries ◽  
Relaxing Effect ◽  
Endothelium Dependent Relaxation ◽  
Stabilization Period

Objective To describe and to characterize the relaxing effect of an extract of the bark of Combretum leprosum on isolated arterial rings from different animals.Methods Rings (3 to 4mm) from rabbit, rat, or porcine arteries rings were suspended in an organ bath (Krebs, 37°C, 95%O2/5%CO2) to record isometric contractions. After the stabilization period (2 to 3 hours) contractions were induced by the addition of phenylephrine (0.1 to 0.3µM) or U46619 (10 to 100nM), and Combretum leprosum extract was added on the plateau of the contractions. Experiments were performed to determine the potency, duration, reversibility, and to get insights on the potential mechanism involved in extract-induced relaxations.Results In all rings tested, Combretumleprosum extract (1.5μg/mL) was able to cause relaxations, which were strictly endothelium-dependent. In rabbit or rat thoracic aorta rings, the relaxations were reversed by vitamin B12a or L-NG-nitroarginine. In porcine right coronary arteries and rabbit abdominal aorta, extract caused both L-NG-nitroarginine-sensitive and L-NG-nitroarginine-resistant relaxations. In rabbit thoracic aorta, the extract was relatively potent (EC50=0.20µg/mL) and caused relaxations; intriguingly the endothelium continued to produce relaxing factors for a long period after removing the extract. The magnitude of extract-induced relaxations was significantly reduced in the absence of extracellular Ca2+; in addition, the TRPs channels blocker ruthenium red (10µM) was able to revert extract-induced relaxations. Phytochemical analyses indicated that the extract was rich in polyphenol-like reacting substances.ConclusionsCombretum leprosum extract contains bioactive compounds capable of promoting Ca2+-dependent stimulation of endothelial cells which results in a prolonged production of relaxing factors.

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