P9.06EVIDENCE FOR A ROLE OF THE VASCULAR ENDOTHELIUM IN THE REGULATION OF ARTERIAL WALL VISCOSITY IN VIVO IN HUMANS

2009 ◽  
Vol 3 (4) ◽  
pp. 168
Author(s):  
J. Bellien ◽  
M. Iacob ◽  
C. Thuillez ◽  
R. Joannides
Keyword(s):  
Vascular Endothelium ◽  
Arterial Wall ◽  
Arterial Wall Viscosity

scholarly journals Evidence for a Role of Vascular Endothelium in the Control of Arterial Wall Viscosity in Humans

Hypertension ◽  
2018 ◽  
Vol 71 (1) ◽  
pp. 143-150 ◽  
Author(s):  
Frederic Roca ◽  
Michele Iacob ◽  
Isabelle Remy-Jouet ◽  
Jeremy Bellien ◽  
Robinson Joannides
Keyword(s):  
Vascular Endothelium ◽  
Arterial Wall ◽  
Arterial Wall Viscosity

scholarly journals Catestatin (chromogranin A344-364) is a novel cardiosuppressive agent: inhibition of isoproterenol and endothelin signaling in the frog heart

2008 ◽  
Vol 295 (1) ◽  
pp. H113-H122 ◽  
Author(s):  
Rosa Mazza ◽  
Alfonsina Gattuso ◽  
Cinzia Mannarino ◽  
Bhawanjit K. Brar ◽  
Sandra Francesca Barbieri ◽  
...  
Keyword(s):  
Vascular Endothelium ◽  
Positive Inotropic Effect ◽  
Threshold Concentration ◽  
Frog Heart ◽  
Stroke Work ◽  
Inotropic Action ◽  
Oxide Synthase ◽  
Endocardial Endothelium

The catecholamine release-inhibitory catestatin [Cts; human chromogranin (Cg) A352-372, bovine CgA344-364] is a vasoreactive and anti-hypertensive peptide derived from CgA. Using the isolated avascular frog heart as a bioassay, in which the interactions between the endocardial endothelium and the subjacent myocardium can be studied without the confounding effects of the vascular endothelium, we tested the direct cardiotropic effects of bovine Cts and its interaction with β-adrenergic (isoproterenol, ISO) and endothelin-1 (ET-1) signaling. Cts dose-dependently decreased stroke volume and stroke work, with a threshold concentration of 11 nM, approaching the in vivo level of the peptide. Cts reduced contractility by inhibiting phosphorylation of phospholamban (PLN). Furthermore, the Cts effect was abolished by pretreatment with either nitric oxide synthase ( NG-monomethyl-l-arginine) or guanylate cyclase (ODQ) inhibitors, or an ETB receptor (ETBR) antagonist (BQ-788). Cts also noncompetitively inhibited the positive inotropic action of ISO. In addition, Cts inhibited the positive inotropic effect of ET-1, mediated by ETA receptors, and did not alter the negative inotropic ET-1 influence mediated by ETBR. Cts action through ETBR was further suggested when, in the presence of BQ-788, Cts failed to inhibit the positive inotropism of both ISO and ET-1 stimulation and PLN phosphorylation. We concluded that the cardiotropic actions of Cts, including the β-adrenergic and ET-1 antagonistic effects, support a novel role of this peptide as an autocrine-paracrine modulator of cardiac function, particularly when the stressed heart becomes a preferential target of both adrenergic and ET-1 stimuli.

scholarly journals Adipocyte-Endothelium Crosstalk in Obesity

2021 ◽  
Vol 12 ◽  
Author(s):  
Rugivan Sabaratnam ◽  
Per Svenningsen
Keyword(s):  
Metabolic Disease ◽  
Endothelial Cells ◽  
Blood Flow ◽  
Vascular Endothelium ◽  
Energy Homeostasis ◽  
Cell Communication ◽  
Normal Organ ◽  
Arterial Endothelial Cells

Obesity is characterized by pathological adipose tissue (AT) expansion. While healthy AT expansion enhances systemic insulin sensitivity, unhealthy AT expansion through increased adipocyte size is associated with insulin resistance, fibrosis, hypoxia, and reduced adipose-derived adiponectin secretion. The mechanisms causing the unhealthy AT expansion are not fully elucidated; yet, dysregulated crosstalk between cells within the AT is an important contributor. Evidence from animal and human studies suggests a crucial role of the crosstalk between vascular endothelium (the innermost cell type in blood vessels) and adipocytes for metabolic homeostasis. Arterial endothelial cells are directly involved in maintaining normal organ functions through local blood flow regulation. The endothelial-dependent regulation of blood flow in AT is hampered in obesity, which negatively affects the adipocyte. Moreover, endothelial cells secrete extracellular vesicles (EVs) that target adipocytes in vivo. The endothelial EVs secretion is hampered in obesity and may be affected by the adipocyte-derived adipokine adiponectin. Adiponectin targets the vascular endothelium, eliciting organ-protective functions through binding to T-cadherin. The reduced obesity-induced adiponectin binding of T-cadherin reduces endothelial EV secretion. This affects endothelial health and cell-cell communication between AT cells and distant organs, influencing systemic energy homeostasis. This review focuses on the current understanding of endothelial and adipocyte crosstalk. We will discuss how obesity changes the AT environment and how these changes contribute to obesity-associated metabolic disease in humans. Particularly, we will describe and discuss the EV-dependent communication and regulation between adipocytes, adiponectin, and the endothelial cells regulating systemic energy homeostasis in health and metabolic disease in humans.

Role of the Liver and Kidney in the Desulphation of Heparin in vivo

1995 ◽  
Vol 74 (02) ◽  
pp. 667-672 ◽  
Author(s):  
Xanthe E Wells ◽  
Joan Dawes
Keyword(s):  
Vascular Endothelium ◽  
Gel Filtration ◽  
High Dose ◽  
Concomitant Increase ◽  
Major Site ◽  
Liver And Kidney ◽  
Sulphated Glycosaminoglycans ◽  
Carbohydrate Chains

SummaryHeparin radiolabelled with 125I was given intravenously to intact, bilaterally nephrectomised or completely hepatectomised rats in the presence and absence of 1 mg unlabelled heparin/kg. Plasma samples were collected and analysed by gel filtration chromatography and affinity chromatography on Polybrene-Sepharose, which binds sulphated glycosaminoglycans. Radiolabel in the plasma was associated with both intact heparin and fully desulphated macromolecular carbohydrate chains. Levels of intact heparin in plasma from control rats decreased with time at both doses with a concomitant increase in desulphated material. Livers accumulated the greatest amounts of radiolabel on a per organ basis. Hepatectomy both increased levels of radiolabel in plasma and decreased amounts of desulphated heparin produced, indicating that the liver was the major site of desulphation. Even after removal of the liver, the desulphated metabolite comprised approximately 15% of radiolabelled material at all times and doses, suggesting an additional site of GAG desulphation which may be the vascular endothelium. The kidneys contributed significantly to in vivo desulphation of heparin only at the high dose.

Role of the vascular endothelium in O2 extraction during progressive ischemia in canine skeletal muscle

1995 ◽  
Vol 79 (4) ◽  
pp. 1351-1360 ◽  
Author(s):  
S. E. Curtis ◽  
B. Vallet ◽  
M. J. Winn ◽  
J. B. Caufield ◽  
C. E. King ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Vascular Endothelium ◽  
Microvascular Endothelium ◽  
Treatment Groups ◽  
O2 Extraction ◽  
O2 Supply ◽  
O2 Delivery

O2 extraction during progressive ischemia in canine skeletal muscle, J. Appl. Physiol. 79(4): 1351–1360, 1995.--O2 uptake (VO2) is defended during decreased O2 delivery (QO2) by an increase in the O2 extraction ratio (O2ER, VO2/QO2), presumably by recruitment of capillaries. This study tested the hypothesis that activity of the microvascular endothelium plays a necessary role in achievement of maximal O2ER. We pump perfused the vascularly isolated hindlimbs of 24 anesthetized and paralyzed dogs at progressively lower flows over a 90-min period. In eight dogs, hindlimb vascular endothelium was removed by injection of deoxycholate (DOC) into the perfusing artery before the ischemic challenge. DOC treatment resulted in loss of normal in vivo and in vitro endothelium-dependent dilatory responses to acetylcholine, but endothelium-independent vascular smooth muscle responses were intact. Eight other dogs were pretreated with nitro-L-arginine methyl ester plus indomethacin (L+I group) to block the synthesis of the vasodilators nitric oxide and prostacyclin. L+I and DOC treatment were associated with increases in hindlimb vascular resistance of 168 +/- 17 and 63 +/- 12%, respectively. O2ER at critical QO2 (QO2 at which VO2 begins to decrease) was 81 +/- 2% in eight control dogs, 66 +/- 6% in L+I, and 42 +/- 4% in DOC, indicating a significant O2 extraction defect in the two treatment groups. These data suggest that products of the vascular endothelium play an important role in the matching of O2 supply to demand during supply limitation in skeletal muscle.

scholarly journals 2424 The role of the retinal vascular endothelium in cellular trafficking in EAU in vivo

1995 ◽  
Vol 35 ◽  
pp. S113
Author(s):  
G.R. Wallace ◽  
D. Williams ◽  
R. Whiston ◽  
J. Biggerstaff ◽  
G.F. Savidge ◽  
...  
Keyword(s):  
Vascular Endothelium ◽  
Cellular Trafficking

scholarly journals Beneficial Role of Vitexin and Isovitexin Flavonoids in the Vascular Endothelium and Cardiovascular System

2020 ◽  
Vol 01 ◽  
Author(s):  
Sharon O. Azubuike-Osu ◽  
Ikenna C. Ohanenye ◽  
Claus Jacob ◽  
Chukwunonso E.C.C. Ejike ◽  
Chibuike C. Udenigwe
Keyword(s):  
Vascular Endothelium ◽  
Cardiovascular Health ◽  
Perfusion Pressure ◽  
Vascular System ◽  
Therapeutic Agents ◽  
Pharmacological Effects ◽  
Medicinal Products

Abstract: Various medicinal plants contain phenolic compounds, which are useful in the treatment of many disease conditions. Particularly, vitexin and its isomer, isovitexin, possess many pharmacological effects including antioxidant, anti-inflammatory, anticancer, antidiabetic, neuroprotective, and antinociceptive activities. Current research has provided evidence for the prospective use of vitexin and isovitexin in the formulation of medicinal products useful in the prevention and treatment of specific ailments. The aim of this review was therefore to examine the influence of vitexin and isovitexin on the vascular system as well as the possible mechanisms through which the flavonoids exert their effects. The review also discussed the importance of vitexin and isovitexin in cardiovascular health through the vascular endothelium. In vivo and in vitro studies suggest that vitexin and isovitexin play a cardioprotective role during ischaemic reperfusion injury and angiogenesis, while isovitexin decreases perfusion pressure and increases the bioavailability of nitric oxide. Taken together, vitexin and isovitexin are promising as therapeutic agents for the formulation of nutraceuticals for the prevention, management and treatment of cardiovascular diseases.

Mitochondrial matrix calcium ions regulate energy production in myocardium: A cytochemical study

1990 ◽  
Vol 48 (2) ◽  
pp. 166-167
Author(s):  
W.A. Jacob ◽  
R. Hertsens ◽  
A. Van Bogaert ◽  
M. De Smet
Keyword(s):  
Energy Metabolism ◽  
Calcium Ions ◽  
Energy Production ◽  
Regulation Of Respiration ◽  
Free Calcium ◽  
Mitochondrial Matrix ◽  
Cytochemical Study ◽  
Nmr Techniques

In the past most studies of the control of energy metabolism focus on the role of the phosphorylation potential ATP/ADP.Pi on the regulation of respiration. Studies using NMR techniques have demonstrated that the concentrations of these compounds for oxidation phosphorylation do not change appreciably throughout the cardiac cycle and during increases in cardiac work. Hence regulation of energy production by calcium ions, present in the mitochondrial matrix, has been the object of a number of recent studies.Three exclusively intramitochondnal dehydrogenases are key enzymes for the regulation of oxidative metabolism. They are activated by calcium ions in the low micromolar range. Since, however, earlier estimates of the intramitochondnal calcium, based on equilibrium thermodynamic considerations, were in the millimolar range, a physiological correlation was not evident. The introduction of calcium-sensitive probes fura-2 and indo-1 made monitoring of free calcium during changing energy metabolism possible. These studies were performed on isolated mitochondria and extrapolation to the in vivo situation is more or less speculative.

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