Displaying publications 41 - 60 of 134 in total

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  1. Cytotoxicity analysis of poly (carbonate-siloxane-urea) urethane
    Kannan RY, Sales KM, Salacinski HJ, Butler PE, Seifalian AM
    Med J Malaysia, 2004 May;59 Suppl B:99-100.
    PMID: 15468837
    Matched MeSH terms: Endothelium, Vascular/drug effects*
  2. Fulltext Biomarkers of severe dengue disease - a review
    John DV, Lin YS, Perng GC
    J Biomed Sci, 2015;22:83.
    PMID: 26462910 DOI: 10.1186/s12929-015-0191-6
    Dengue virus infection presents a wide spectrum of manifestations including asymptomatic condition, dengue fever (DF), or severe forms, such as dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS) in affected individuals. The early prediction of severe dengue in patients without any warning signs who may later develop severe DHF is very important to choose appropriate intensive supportive therapy since available vaccines for immunization are yet to be approved. Severe dengue responses include T and B cell activation and apoptosis, cytokine storm, hematologic disorders and complement activation. Cytokines, complement and other unidentified factors may transiently act on the endothelium and alter normal fluid barrier function of the endothelial cells and cause plasma leakage. In this review, the host factors such as activated immune and endothelial cells and their products which can be utilized as biomarkers for severe dengue disease are discussed.
    Matched MeSH terms: Endothelium, Vascular/metabolism*
  3. Effects of 1α-Calcidol (Alfacalcidol) on Microvascular Endothelial Function, Arterial Stiffness, and Blood Pressure in Type II Diabetic Nephropathy Patients
    Munisamy S, Daud KM, Mokhtar SS, Rasool AH
    Microcirculation, 2016 Jan;23(1):53-61.
    PMID: 26749451 DOI: 10.1111/micc.12256
    To determine the effects of six months alfacalcidol on microvascular endothelial function, arterial stiffness, and BP in DN patients.
    Matched MeSH terms: Endothelium, Vascular/physiopathology*
  4. Endothelium dependent hyperpolarization-type relaxation compensates for attenuated nitric oxide-mediated responses in subcutaneous arteries of diabetic patients
    Mokhtar SS, Vanhoutte PM, Leung SW, Yusof MI, Wan Sulaiman WA, Mat Saad AZ, et al.
    Nitric Oxide, 2016 Feb 29;53:35-44.
    PMID: 26768833 DOI: 10.1016/j.niox.2015.12.007
    Diabetes impairs endothelium-dependent relaxations. The present study evaluated the contribution of different endothelium-dependent relaxing mechanisms to the regulation of vascular tone in subcutaneous blood vessels of humans with Type 2 diabetes mellitus. Subcutaneous arteries were isolated from tissues of healthy controls and diabetics. Vascular function was determined using wire myography. Expressions of proteins were measured by Western blotting and immunostaining. Endothelium-dependent relaxations to acetylcholine were impaired in arteries from diabetics compared to controls (P = 0.009). Acetylcholine-induced nitric oxide (NO)-mediated relaxations [in the presence of an inhibitor of cyclooxygenases (COX; indomethacin) and small and intermediate conductance calcium-activated potassium channel blockers (UCL1684 and TRAM 34, respectively)] were attenuated in arteries from diabetics compared to controls (P endothelium-dependent hyperpolarization (EDH)-type relaxations [in the presence of indomethacin and the NO synthase blocker, l-NAME] were augmented in arteries from diabetics compared to controls (P = 0.003). Endothelium-independent relaxations to sodium nitroprusside (NO donor) and salbutamol (β-adrenoceptor agonist) were preserved, but those to prostacyclin were attenuated in diabetics compared to controls (P = 0.017). In arteries of diabetics, protein expressions of endothelial NO synthase, prostacyclin synthase and prostacyclin receptors were decreased, but those of COX-2 were increased. These findings suggest that in human diabetes, the impairment of endothelium-dependent relaxations is caused by a diminished NO bioavailability; however, EDH appears to compensate, at least in part, for this dysfunction.
    Matched MeSH terms: Endothelium, Vascular/metabolism*
  5. Could hypertension possibly be adaptive?
    Prakash ES, Fink GD
    Clin Exp Pharmacol Physiol, 2010 Feb;37(2):e99-e106.
    PMID: 19719749 DOI: 10.1111/j.1440-1681.2009.05284.x
    1. We believe that the ultimate goal of cardiovascular regulatory mechanisms is not the regulation of arterial blood pressure (BP), but the maintenance of tissue blood flows commensurate with metabolic requirements. Thus, elevated BP can potentially contribute to optimizing tissue blood flows under select circumstances; for example, when there are primary defects in autoregulation of tissue blood flows. 2. The hypothesis that a primary defect in autoregulation of tissue blood flows may be responsible for the development of hypertension is presented. It is argued that, in this context, at least part of the rise in BP may be reflexly driven by a 'metaboreflex', a homeostatic mechanism acting to regulate tissue blood flows. 3. We argue that in the context of primary defects in autoregulation of tissue blood flows, the ability to generate and sustain a hypertensive phenotype increases the lifespan of species (i.e. if it were not for this adaptive hypertensive phenotype, death due to circulatory failure would occur much earlier). 4. Experimental and clinical evidence that indirectly supports the hypothesis is reviewed briefly and a means for testing this hypothesis is suggested.
    Matched MeSH terms: Endothelium, Vascular/physiopathology
  6. Fulltext A prospective analysis of corneal endothelial polymegethism and cell density in young adult Asians
    Doughty MJ
    Clin Exp Optom, 2014 May;97(3):256-63.
    PMID: 24405014 DOI: 10.1111/cxo.12127
    PURPOSE: The aim was to assess the morphology of the Asian corneal endothelium, particularly the index of polymegethism and its relationship to endothelial cell density assessments.
    METHODS: The central regions of the corneal endothelium of 72 healthy, normal weight, non-contact lens wearers were assessed by non-contact specular microscopy. There were six groups of persons, aged between 18 and 27 years, whose ethnic origins were self-reported as Asian (Mainland China, Hong Kong, India, Malaysia, Pakistan or other Asian groups). Single images including at least 100 contiguous cells were obtained from each subject and were processed by planimetry after manual border marking to minimise errors. Calculations were made of the coefficient of variation of cell area (COV; polymegethism) as well as the endothelial cell density and percentage of six-sided cells.
    RESULTS: The COV values ranged from 18 to 30.4 per cent (group mean 24.5 ± 2.8 per cent). The corneas had essentially normal thickness (0.530 ± 0.026 mm), with the endothelia showing a high percentage of six-sided cells (66.3 ± 7.1 per cent) and none showing even mild signs of polymegethism. Endothelial cell density estimates based on average cell areas ranged from 2,020 to 3,623 cells per mm(2) and from 2,157 to 3,835 with calculations based on individual cell areas. The difference between the two estimates of endothelial cell density was strongly related to the coefficient of variation (r = 0.765).
    CONCLUSIONS: This result is consistent with several older reports indicating that it is uncommon to find polymegethism in healthy young adult Asian individuals. Nonetheless, even low coefficient of variation values can substantially affect the estimations of the cell density.
    KEYWORDS: Asian; cornea; endothelium; human; polymegathism
    Matched MeSH terms: Endothelium, Corneal/cytology*
  7. Lipid peroxidation in the descending thoracic aorta of rats deprived of REM sleep using the inverted flowerpot technique
    Nawi A, Eu KL, Faris ANA, Wan Ahmad WAN, Noordin L
    Exp Physiol, 2020 08;105(8):1223-1231.
    PMID: 32539237 DOI: 10.1113/EP088667
    NEW FINDINGS: What is the central question of this study? Deprivation of rapid eye movement (REM) sleep is associated with increased oxidative stress, but its effects on the blood vessels are poorly documented. We investigated whether REM sleep deprivation induces oxidative stress and causes lipid peroxidation in the aorta. What is the main finding and its important? We demonstrate that REM sleep deprivation induces oxidative stress and mediates lipid peroxidation in the aorta. This can cause endothelial changes and increased blood pressure. These findings will contribute to the growing body of literature on the mechanism underlying the effects of sleep deprivation on cardiovascular disease.

    ABSTRACT: Oxidative stress-mediated lipid peroxidation is a known cause of endothelial injury or dysfunction. Deprivation of rapid eye movement (REM) sleep is associated with oxidative stress. To date, the pathogenesis of increased blood pressure after sleep deprivation remains poorly understood, particularly in the REM sleep phase. Our aim was to investigate the effects of REM sleep deprivation on blood vessels in the REM sleep-deprived rat model. Twenty-eight male Sprague-Dawley rats were divided into four equal groups: free-moving control rats, rats deprived of REM sleep for 72 h (REMsd), tank control rats and 72 h sleep-recovered rats after 72 h of REM sleep deprivation. The rats were deprived of REM sleep using the inverted flowerpot technique. Food consumption, body weight gain and systolic blood pressure were monitored. At the end of the experiment, the descending thoracic aorta was isolated for the measurement of oxidative stress markers. Despite a significant increase in food consumption in the REMsd group compared with the other groups, there was a significant reduction in body weight gain. Systolic blood pressure also showed a significant increase in the REMsd group compared with the other groups. Superoxide dismutase activity was significantly lower and malondialdehyde concentrations significantly higher in the REMsd group compared with the other groups. Increased levels of malondialdehyde are suggestive of lipid peroxidation in the blood vessels, and oxidative stress may be attributed to the initiation of the process. The changes after REM sleep deprivation revert during sleep recovery. In conclusion, the findings of the present study provide convincing evidence that REM sleep deprivation induced lipid peroxidation, leading to endothelial damage.

    Matched MeSH terms: Endothelium, Vascular/physiopathology*
  8. Mechanism of vasorelaxation induced by eupatorin in the rats aortic ring
    Yam MF, Tan CS, Ahmad M, Shibao R
    Eur J Pharmacol, 2016 Oct 15;789:27-36.
    PMID: 27370961 DOI: 10.1016/j.ejphar.2016.06.047
    Previous studies demonstrated that eupatorin content in Orthosiphon stamineus fractions correlated with their vasorelaxation activity. Even with previous studies, there is still very little information on the vasorelaxation effect of eupatorin, and not many scientific studies had been carried out. Therefore, the present study was designed to investigate the vasorelaxation activity and mechanism of action of eupatorin. The vasorelaxation activity and the underlying mechanisms of eupatorin was evaluated on thoracic aortic rings isolated from Sprague Dawley rats. Eupatorin caused the relaxation of aortic rings pre-contracted with phenylephrine with and without endothelium (pD2=6.66±0.13, EMAX=99.72±6.39%; pD2=6.10±0.22, EMAX=65.78±8.01%), and also the relaxation of endothelium-intact aortic rings pre-contracted with potassium chloride (pD2=6.20±0.30, EMAX=71.89±12.25%). In the presence of Nω-nitro-l-arginine methyl ester (pD2<4.60, EMAX=24.91±6.39%), methylene blue (pD2=6.05±0.38, EMAX=66.79±9.69%), ODQ (pD25.84±0.32, EMAX=60.47±9.6%), indomethacin (pD2=6.27±0.21, EMAX=76.03±9.45%), tetraethylammonium (pD2=6.09±0.35, EMAX=69.35±11.31%), 4-aminopyridine (pD2=6.34±0.12, EMAX=76±6.1%), barium chloride (pD2=6.47±0.14, EMAX=79.61±10.02%), atropine (pD2=6.36±0.29, EMAX=86.47±12.95%) and propranolol (pD2=6.49±0.26, EMAX=83.2±12.01%), relaxation stimulated by eupatorin was significantly reduced. Eupatorin was also found to be active in reducing Ca(2+) release from sarcoplasmic reticulum and in blocking calcium channels. The present study demonstrates the vasorelaxation effect of eupatorin involving NO/sGC/cGMP and indomethacin pathways, calcium and potassium channels, and muscarinic and beta-adrenergic receptors.
    Matched MeSH terms: Endothelium, Vascular/drug effects
  9. Fulltext Epigallocatechin gallate (EGCG) alleviates vascular dysfunction in angiotensin II-infused hypertensive mice by modulating oxidative stress and eNOS
    Mohd Sabri NA, Lee SK, Murugan DD, Ling WC
    Sci Rep, 2022 Oct 21;12(1):17633.
    PMID: 36271015 DOI: 10.1038/s41598-022-21107-5
    Epigallocatechin gallate (EGCG) has been shown to have antihypertensive activity. However, the role of epigallocatechin gallate (EGCG) in improving vascular function via modulation of endothelial nitric oxide synthase (eNOS) in hypertensive subjects is not well researched. Angiotensin II-infused hypertensive mice (8-10 weeks old) received EGCG (50 mg/kg/day) for 14 days via oral gavage. The arterial systolic blood pressure (SBP) was measured using the tail-cuff method every three days. At the end of the treatment, the vascular reactivity of the isolated aortae was studied using wire myographs. The level of nitric oxide (NO), cyclic guanosine monophosphate (cGMP) and tetrahydrobiopterine (BH4) were determined using assay kits while the presence of proteins (NOS, p-eNOS and NOx-2) were determined using by Western blotting. In vivo treatment with EGCG for 14 days significantly attenuated the increase in SBP, alleviated the vascular dysfunction, increased the vascular cGMP and BH4 level as well as the expression of p-eNOS and decreased elevated ROS level and NOx-2 protein in angiotensin II-infused hypertensive mice. Collectively, treatment with EGCG in hypertensive mice exerts a blood pressure lowering effect which is partly attributed to the improvement in the vascular function due to its ability to reduce vascular oxidative stress in the aortic tissue leading to a decrease in eNOS uncoupling thus increasing NO bioavailability.
    Matched MeSH terms: Endothelium, Vascular/metabolism
  10. Fulltext Endothelial glycocalyx degradation and disease severity in Plasmodium vivax and Plasmodium knowlesi malaria
    Barber BE, Grigg MJ, Piera KA, Chen Y, William T, Weinberg JB, et al.
    Sci Rep, 2021 May 07;11(1):9741.
    PMID: 33963210 DOI: 10.1038/s41598-021-88962-6
    Degradation of the endothelial glycocalyx is associated with mortality in adult falciparum malaria. However, its role in the pathogenesis of non-falciparum malaria is unknown. In Malaysian patients with knowlesi (n = 200) and vivax (n = 61) malaria, and in healthy controls (n = 50), we measured glycocalyx breakdown products plasma syndecan-1 and urinary glycosaminoglycans, and evaluated correlations with biomarkers of disease severity. Urinary glycosaminoglycans were increased in patients with knowlesi and vivax malaria compared to healthy controls, and in knowlesi malaria were highest in those with severe disease. In knowlesi malaria, plasma syndecan-1 was also highest in those with severe disease, and correlated with markers of endothelial activation (angiopoietin-2, osteoprotegerin, ICAM-1), asymmetric dimethylarginine (ADMA) and impaired microvascular reactivity. Syndecan-1 also correlated with endothelial activation (ICAM-1, angiopoietin-2) and ADMA in vivax malaria. In knowlesi malaria increased syndecan-1 was associated with acute kidney injury, after controlling for age and parasitemia. In knowlesi malaria, the difference in median syndecan-1 between severe and non-severe disease was more marked in females than males. Endothelial glycocalyx degradation is increased in knowlesi and vivax malaria, and associated with disease severity and acute kidney injury in knowlesi malaria. Agents that inhibit glycocalyx breakdown may represent adjunctive therapeutics for severe non-falciparum malaria.
    Matched MeSH terms: Endothelium, Vascular/metabolism*
  11. The aporphine alkaloid boldine improves endothelial function in spontaneously hypertensive rats
    Lau YS, Machha A, Achike FI, Murugan D, Mustafa MR
    Exp Biol Med (Maywood), 2012 Jan;237(1):93-8.
    PMID: 22156043 DOI: 10.1258/ebm.2011.011145
    Boldine, a major aporphine alkaloid found in Chilean boldo tree, is a potent antioxidant. Oxidative stress plays a detrimental role in the pathogenesis of endothelial dysfunction in hypertension. In the present study, we investigated the effects of boldine on endothelial dysfunction in hypertension using spontaneously hypertensive rats (SHR), the most studied animal model of hypertension. SHR and their age-matched normotensive Wistar-Kyoto (WKY) rats were treated with boldine (20 mg/kg per day) or its vehicle, which served as control, for seven days. Control SHR displayed higher systolic blood pressure (SBP), reduced endothelium-dependent aortic relaxation to acetylcholine (ACh), marginally attenuated endothelium-independent aortic relaxation to sodium nitroprusside (SNP), increased aortic superoxide and peroxynitrite production, and enhanced p47(phox) protein expression as compared with control WKY rats. Boldine treatment significantly lowered SBP in SHR but not in WKY. Boldine treatment enhanced the maximal relaxation to ACh in SHR, but had no effect in WKY, whereas the sensitivity to ACh was increased in both SHR and WKY aortas. Boldine treatment enhanced sensitivity, but was without effect on maximal aortic relaxation responses, to SNP in both WKY and SHR aortas. In addition, boldine treatment lowered aortic superoxide and peroxynitrite production and downregulated p47(phox) protein expression in SHR aortas, but had no effect in the WKY control. These results show that boldine treatment exerts endothelial protective effects in hypertension, achieved, at least in part, through the inhibition of NADPH-mediated superoxide production.
    Matched MeSH terms: Endothelium, Vascular/drug effects*; Endothelium, Vascular/physiopathology
  12. Mechanisms of the anti-hypertensive effect of Hibiscus sabdariffa L. calyces
    Ajay M, Chai HJ, Mustafa AM, Gilani AH, Mustafa MR
    J Ethnopharmacol, 2007 Feb 12;109(3):388-93.
    PMID: 16973321
    Previous studies have demonstrated the anti-hypertensive effects of Hibiscus sabdariffa L. (HS) in both humans and experimental animals. To explore the mechanisms of the anti-hypertensive effect of the HS, we examined the effects of a crude methanolic extract of the calyces of HS (HSE) on vascular reactivity in isolated aortas from spontaneously hypertensive rats. HSE relaxed, concentration-dependently, KCl (high K(+), 80 mM)- and phenylephrine (PE, 1 microM)-pre-contracted aortic rings, with a greater potency against the alpha(1)-adrenergic receptor agonist. The relaxant effect of HSE was partly dependent on the presence of a functional endothelium as the action was significantly reduced in endothelium-denuded aortic rings. Pretreatment with atropine (1 microM), L-NAME (10 microM) or methylene blue (10 microM), but not indomethacin (10 microM), significantly blocked the relaxant effects of HSE. Endothelium-dependent and -independent relaxations induced by acetylcholine and sodium nitroprusside, respectively, were significantly enhanced in aortic rings pretreated with HSE when compared to those observed in control aortic rings. The present results demonstrated that HSE has a vasodilator effect in the isolated aortic rings of hypertensive rats. These effects are probably mediated through the endothelium-derived nitric oxide-cGMP-relaxant pathway and inhibition of calcium (Ca(2+))-influx into vascular smooth muscle cells. The present data further supports previous in vivo findings and the traditional use of HS as an anti-hypertensive agent.
    Matched MeSH terms: Endothelium, Vascular/drug effects; Endothelium, Vascular/physiopathology
  13. Contractile function of smooth muscle retained after overnight storage
    Loong BJ, Tan JH, Lim KH, Mbaki Y, Ting KN
    Naunyn Schmiedebergs Arch Pharmacol, 2015 Oct;388(10):1061-7.
    PMID: 26051407 DOI: 10.1007/s00210-015-1140-3
    The functional responses of different overnight-stored in vitro tissues are not clearly described in any animal model. The influence of overnight storage in an animal model may vary between tissue types. We employed Sprague-Dawley rat as our animal model and investigated the functional changes of rat aorta, trachea, bronchus and bladder that were used (i) immediately after surgical removal (denoted as fresh) and (ii) after storage in aerated (95% O2, 5% CO2) Krebs-Ringer bicarbonate solution at 4 °C for 24 h (denoted as stored). The aorta ring was pre-contracted with phenylephrine, and the functional response of the tissue was investigated using isoprenaline, forskolin and carbachol. Carbachol was also used to increase the tone in trachea, bronchus rings and bladder strips. A clear reduced function of endothelium, with a minor if any effect in the smooth muscle function in rat aorta was observed after overnight storage. The contractile response of overnight-stored rat airway (trachea and bronchus) and bladder smooth muscles remained unchanged. Among all tested tissues, only bronchus showed a reduced response rate (only 40% responded) after storage. In vitro rat tissues that are stored in Krebs solution at 4 °C for 24 h can still be used to investigate smooth muscle responses, however, not endothelium-mediated responses for aorta. The influence of overnight storage on different tissues from an animal model (Sprague-Dawley rat in our study) also provides an insight in maximising the use of sacrificed animals.
    Matched MeSH terms: Endothelium, Vascular/drug effects*; Endothelium, Vascular/metabolism
  14. Treatment with salvianolic acid B restores endothelial function in angiotensin II-induced hypertensive mice
    Ling WC, Liu J, Lau CW, Murugan DD, Mustafa MR, Huang Y
    Biochem Pharmacol, 2017 Jul 15;136:76-85.
    PMID: 28396195 DOI: 10.1016/j.bcp.2017.04.007
    Salvianolic acid B (Sal B) is one of the most abundant phenolic acids derived from the root of Danshen with potent anti-oxidative properties. The present study examined the vasoprotective effect of Sal B in hypertensive mice induced by angiotensin II (Ang II). Sal B (25mg/kg/day) was administered via oral gavage for 11days to Ang II (1.2mg/kg/day)-infused C57BL/6J mice (8-10weeks old). The vascular reactivity (both endothelium-dependent relaxations and contractions) in mouse arteries was examined by wire myography. The production of reactive oxygen species (ROS), protein level and localization of angiotensin AT1 receptors and the proteins involved in ROS formation were evaluated using dihydroethidium (DHE) fluorescence, lucigenin-enhanced chemiluminescence, immunohistochemistry and Western blotting, respectively. The changes of ROS generating proteins were also assessed in vitro in human umbilical vein endothelial cells (HUVECs) exposed to Ang II with and without co-treatment with Sal B (0.1-10nM). Oral administration of Sal B reversed the Ang II-induced elevation of arterial systolic blood pressure in mice, augmented the impaired endothelium-dependent relaxations and attenuated the exaggerated endothelium-dependent contractions in both aortas and renal arteries of Ang II-infused mice. In addition, Sal B treatment normalized the elevated levels of AT1 receptors, NADPH oxidase subunits (NOx-2 and NOx-4) and nitrotyrosine in arteries of Ang II-infused mice or in Ang II-treated HUVECs. In summary, the present study provided additional evidence demonstrating that Sal B treatment for 11days reverses the impaired endothelial function and with a marked inhibition of AT1 receptor-dependent vascular oxidative stress. This vasoprotective and anti-oxidative action of Sal B most likely contributes to the anti-hypertensive action of the plant-derived compound.
    Matched MeSH terms: Endothelium, Vascular/drug effects; Endothelium, Vascular/physiology*
  15. Chronic treatment with flavonoids prevents endothelial dysfunction in spontaneously hypertensive rat aorta
    Machha A, Mustafa MR
    J Cardiovasc Pharmacol, 2005 Jul;46(1):36-40.
    PMID: 15965352
    Flavonoids are known to possess cardioprotective properties. Vascular endothelial function is a surrogate marker for cardiovascular diseases, including hypertension. We have studied the effects of chronic flavonoid treatment on vascular endothelial functions in spontaneously hypertensive rats (SHR). Starting from 6-7 weeks old, SHR were given flavonoids (baicalein, flavone, or quercetin) orally (10 mg/kg, once daily) to the SHRs for 4 weeks. Aortas from all the flavonoid-treated animals showed remarkably higher endothelium-dependent relaxations to acetylcholine, to a similar extent as those pretreated with the angiotensin-converting enzyme inhibitor, captopril. However, in contrast to other experimental groups, flavone pretreatment also enhanced the endothelium-independent relaxations to sodium nitroprusside. In addition, treatment with either flavone or quercetin induced a significant attenuation in systolic blood pressure of the hypertensive animals. The present results suggest that chronic treatment with the flavonoids (baicalein, flavone, and quercetin) preserves vascular endothelial functions in hypertensive animals through several possible actions, including increasing endothelial nitric oxide production and bioavailability and reduction in blood pressure.
    Matched MeSH terms: Endothelium, Vascular/drug effects*; Endothelium, Vascular/physiopathology
  16. Vasodilator effect of Phlomis bracteosa constituents is mediated through dual endothelium-dependent and endothelium-independent pathways
    Khan AU, Ullah R, Khan A, Mustafa MR, Hussain J, Murugan DD, et al.
    Clin Exp Hypertens, 2012;34(2):132-9.
    PMID: 21967029 DOI: 10.3109/10641963.2011.601383
    This study describes the vasorelaxant potential of some pure compounds isolated from Phlomis bracteosa L. marrubiin, phlomeoic acid, and two new constituents labeled as RA and RB. In rat thoracic aortic rings denuded of endothelium, marrubiin, phlomeoic acid, RA, and RB caused relaxation of high K(+) (80 mM) and phenylephrine (1 μM)-induced contractions at the concentration range of 1.0-1000 μg/mL. Marrubiin, phlomeoic acid, RA, and RB concentration dependently (3.0-10 μg/mL) shifted the Ca(++) curves to the right obtained in Ca(++)-free medium. The vasodilator effect of marrubiin, phlomeoic acid, RA, and RB was partially blocked by N(ω)-nitro-L-arginine methyl ester in endothelium-intact aorta preparations. These results reveal that P. bracteosa constituents: marrubiin, phlomeoic acid, RA, and RB exhibit vasodilator action occurred via a combination of endothelium-independent Ca(++) antagonism and endothelium-dependent N(ω)-nitro-L-arginine methyl ester-sensitive nitric oxide-modulating mechanism.
    Matched MeSH terms: Endothelium, Vascular/drug effects; Endothelium, Vascular/physiology
  17. Assessment of macrovascular endothelial function using pulse wave analysis and its association with microvascular reactivity in healthy subjects
    Ibrahim NNIN, Rasool AHG
    Skin Res Technol, 2017 Aug;23(3):321-325.
    PMID: 27868242 DOI: 10.1111/srt.12338
    BACKGROUND: Pulse wave analysis (PWA) and laser Doppler fluximetry (LDF) are non-invasive methods of assessing macrovascular endothelial function and microvascular reactivity respectively. The aim of this study was to assess the correlation between macrovascular endothelial function assessed by PWA and microvascular reactivity assessed by LDF.

    METHOD: 297 healthy and non-smoking subjects (159 females, mean age (±SD) 23.56 ± 4.54 years) underwent microvascular reactivity assessment using LDF followed by macrovascular endothelial function assessments using PWA.

    RESULTS: Pearson's correlation showed no correlation between macrovascular endothelial function and microvascular reactivity (r = -0.10, P = 0.12).

    CONCLUSION: There was no significant correlation between macrovascular endothelial function assessed by PWA and microvascular reactivity assessed by LDF in healthy subjects.

    Matched MeSH terms: Endothelium, Vascular/drug effects; Endothelium, Vascular/physiopathology
  18. Vasorelaxant activities and the underlying pharmacological mechanisms of Gynura procumbens Merr. leaf extracts on rat thoracic aorta
    Iqbal Z, Bello I, Asmawi MZ, Al-Mansoub MA, Ahmad A, Jabeen Q, et al.
    Inflammopharmacology, 2019 Apr;27(2):421-431.
    PMID: 29185178 DOI: 10.1007/s10787-017-0422-4
    Previous studies have investigated the cardiovascular activity of Gynura procumbens Merr. single-solvent extracts. The objective of this study was to evaluate the in vitro vasorelaxant properties and the underlying pharmacological mechanisms of serial extracts and fractions of Gynura procumbens (GP). The leaves of GP were serially extracted with petroleum ether, chloroform, methanol and water using the maceration method. Suspended aortic ring preparations were pre-contracted with phenylephrine (PE 1 µM), followed by cumulative addition of GP extracts (0.25-3 mg/mL). The petroleum ether extract (GPPE) was the most potent among the four extracts. Pre-incubation of endothelium-intact aorta with atropine (1 µM), indomethacin (10 µM), methylene blue (10 µM), propranolol (1 µM) and potassium channel blockers such as TEA (1 µM), glibenclamide (10 µM), 4-aminopyridine (1 µM) and barium chloride (10 mM) had no effect on GPPE-induced vasorelaxation. The vasorelaxant effect of GPPE was partly diminished by pretreatment of aortic rings preparations with L-NAME (10 µM) and even more so in endothelium-denuded aortic rings, indicating a minimal involvement of endothelium-dependent pathway in GPPE-induced vasorelaxation. The calcium-induced vasocontractions were antagonized significantly and concentration-dependently by GPPE in calcium free and high potassium medium. These results illustrate that Ca2+ antagonizing actions of GPPE in rat isolated aorta are comparable to that of verapamil and may be mainly responsible for its vasodilation effect. The antioxidant activity of GPPE supports its vasorelaxant effect by attenuating the production of deleterious free radicals and reactive oxygen species in the vasculature.
    Matched MeSH terms: Endothelium, Vascular/drug effects; Endothelium, Vascular/metabolism
  19. Fulltext 3',4'-dihydroxyflavonol ameliorates endoplasmic reticulum stress-induced apoptosis and endothelial dysfunction in mice
    Lau YS, Mustafa MR, Choy KW, Chan SMH, Potocnik S, Herbert TP, et al.
    Sci Rep, 2018 01 29;8(1):1818.
    PMID: 29379034 DOI: 10.1038/s41598-018-19584-8
    Endoplasmic reticulum (ER) stress has been implicated in the development of hypertension 3 through the induction of endothelial impairment. As 3',4'-dihydroxyflavonol (DiOHF) 4 reduces vascular injury caused by ischaemia/reperfusion or diabetes, and flavonols have been demonstrated to attenuate ER stress, we investigated whether DiOHF can protect mice from ER stress-induced endothelial dysfunction. Male C57BLK/6 J mice were injected with tunicamycin to induce ER stress in the presence or absence of either DiOHF or tauroursodeoxycholic acid (TUDCA), an inhibitor of ER stress. Tunicamycin elevated blood pressure and impaired endothelium-dependent relaxation. Moreover, in aortae there was evidence of ER stress, oxidative stress and reduced NO production. This was coincident with increased NOX2 expression and reduced phosphorylation of endothelial nitric oxide synthase (eNOS) on Ser1176. Importantly, the effects of tunicamycin were significantly ameliorated by DiOHF or TUDCA. DiOHF also inhibited tunicamycin-induced ER stress and apoptosis in cultured human endothelial cells (HUVEC). These results provide evidence that ER stress is likely an important initiator of endothelial dysfunction through the induction of oxidative stress and a reduction in NO synthesis and that DiOHF directly protects against ER stress- induced injury. DiOHF may be useful to prevent ER and oxidative stress to preserve endothelial function, for example in hypertension.
    Matched MeSH terms: Endothelium, Vascular/drug effects*; Endothelium, Vascular/metabolism
  20. Insulin-like growth factor-1 receptor expression in the placentae of diabetic and normal pregnancies
    Hayati AR, Cheah FC, Tan AE, Tan GC
    Early Hum Dev, 2007 Jan;83(1):41-6.
    PMID: 16750336 DOI: 10.1016/j.earlhumdev.2006.04.002
    BACKGROUND: Septal hypertrophic cardiomyopathy (sHCM) is a characteristic anomaly of the infant of diabetic mother (IDM). Insulin-like growth factor-1 (IGF-1) has been identified as a mediator of tissue overgrowth and we have previously shown that maternal IGF-1 levels were significantly elevated among neonates with asymmetrical sHCM. IGF-1 does not cross the placenta; it exerts physiologic action through binding to the IGF-1 receptor (IGF-1R). Localisation and expression of IGF-1R in term diabetic pregnancies are largely unclear. We have studied IGF-1R in the placentae of diabetic and normal pregnancies and this receptor expression in association with neonates with sHCM.
    METHODS: IGF-1R localization and expression in the placentae of six diabetic pregnancies associated with neonatal sHCM were compared with six each of randomly selected diabetic and normal pregnancies without neonatal sHCM by immunohistochemistry. The staining for IGF-1R in the deciduas, cytotrophoblasts, syncytiotrophoblasts and villous endothelium for these 18 samples were assessed and scored by two pathologists who were blinded to the respective diagnoses.
    RESULTS: Placental IGF-1R staining was negative in the villous endothelium for all three groups. IGF-1R staining was present in deciduas, cytotrophoblasts and syncytiotrophoblasts but the staining was weaker in the entire group of infants with sHCM compared to those without sHCM.
    CONCLUSIONS: IGF-1R is localized in all cell types of the placenta except in villous endothelium. Weaker placental IGF-1R staining in the placentae of diabetic pregnancies associated with sHCM suggests reduced expression of IGF-1R. This may be a down-regulatory response to elevated maternal IGF with neonatal sHCM outcome.
    Matched MeSH terms: Endothelium/metabolism; Endothelium/pathology
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