scholarly journals The effect of kisspeptin on the regulation of vascular tone

2015 ◽  
Vol 93 (9) ◽  
pp. 787-791 ◽  
Author(s):  
Zsófia Mezei ◽  
Omid Zamani-Forooshani ◽  
Krisztina Csabafi ◽  
Bence Szikszai ◽  
Eszter Papp ◽  
...  
Keyword(s):  
Vascular Tone ◽  
Eicosanoid Synthesis ◽  
Lipoxygenase Products ◽  
Intracellular Ca ◽  
Prostaglandin F ◽  
Wistar Kyoto ◽  
Layer Chromatography ◽  
Dose Dependent ◽  
Regulation Of Vascular Tone

Kisspeptin has been implicated in cardiovascular control. Eicosanoids play a crucial role in the activation of platelets and the regulation of vascular tone. In the present study, we investigated the effect of kisspeptins on eicosanoid synthesis in platelets and aorta in vitro. Platelets and aorta were isolated from Wistar–Kyoto rats. After preincubation with different doses of kisspeptin, samples were incubated with [1-14C]arachidonic acid (0.172 pmol/mL) in tissue culture Medium 199. The amount of labeled eicosanoids was measured with liquid scintillation, after separation with overpressure thin-layer chromatography. Kisspeptin-13 stimulated the thromboxane synthesis. The dose–response curve was bell-shaped and the most effective concentration was 2.5 × 10−8 mol/L, inducing a 27% increase. Lipoxygenase products of platelets displayed a dose-dependent elevation up to the dose of 5 × 10−8 mol/L. In the aorta, kisspeptin-13 induced a marked elevation in the production of 6-keto-prostaglandin F1α, the stable metabolite of prostacyclin, and lipoxygenase products. Different effects of kisspeptin on cyclooxygenase and lipoxygenase products indicate that beyond intracellular Ca2+ mobilization, other signaling pathways might also contribute to its actions. Our data suggest that kisspeptin, through the alteration of eicosanoid synthesis in platelets and aorta, may play a physiologic and (or) pathologic role in the regulation of vascular tone.

Effects of pinacidil on coronary Ca2+-myosin phosphorylation in cold potassium cardioplegia model

2000 ◽  
Vol 279 (3) ◽  
pp. H882-H888 ◽  
Author(s):  
Naruto Matsuda ◽  
Kathleen G. Morgan ◽  
Frank W. Sellke
Keyword(s):  
Time Course ◽  
Dependent Manner ◽  
Coronary Smooth Muscle ◽  
Intracellular Ca ◽  
No Signaling ◽  
Synthase Inhibitor ◽  
Mlc Phosphorylation ◽  
Dose Dependent ◽  
Cardioplegic Solutions

The effects of the potassium (K+) channel opener pinacidil (Pin) on the coronary smooth muscle Ca2+-myosin light chain (MLC) phosphorylation pathway under hypothermic K+cardioplegia were determined by use of an in vitro microvessel model. Rat coronary arterioles (100–260 μm in diameter) were subjected to 60 min of simulated hypothermic (20°C) K+cardioplegic solutions (K+= 25 mM). We first characterized the time course of changes in intracellular Ca2+concentration, MLC phosphorylation, and diameter and observed that the K+cardioplegia-related vasoconstriction was associated with an activation of the Ca2+-MLC phosphorylation pathway. Supplementation with Pin effectively suppressed the Ca2+accumulation and MLC phosphorylation in a dose-dependent manner and subsequently maintained a small decrease in vasomotor tone. The ATP-sensitive K+(KATP)-channel blocker glibenclamide, but not the nitric oxide (NO) synthase inhibitor Nω-nitro-l-arginine methyl ester, significantly inhibited the effect of Pin. K+cardioplegia augments the coronary Ca2+-MLC pathway and results in vasoconstriction. Pin effectively prevents the activation of this pathway and maintains adequate vasorelaxation during K+cardioplegia through a KATP-channel mechanism not coupled with the endothelium-derived NO signaling cascade.

Influence of SIN-1 on Platelet Ca2+ Handling in Patients with Suspected Coronary Artery Disease: Ex Vivo and In Vitro Studies

2000 ◽  
Vol 83 (05) ◽  
pp. 752-758 ◽  
Author(s):  
Claude Le Feuvre ◽  
Annie Brunet ◽  
Thuc Do Pham ◽  
Jean-Philippe Metzger ◽  
André Vacheron ◽  
...  
Keyword(s):  
Superoxide Anion ◽  
Vascular Tone ◽  
Ex Vivo ◽  
Suspected Coronary Artery Disease ◽  
In Vitro Studies ◽  
H2o2 Formation ◽  
Artery Disease ◽  
Dose Dependent

SummaryThe 3-morpholinosydnonimine (SIN-1) generates both nitric oxide (NO) and superoxide anion (O2−). It elicits dose-dependent vasodilation in vivo, in spite of the opposite effects of its breakdown products on vascular tone and platelet aggregation.This study was designed to investigate the influence of intravenous SIN-1 injection on platelet Ca2+ handling in patients undergoing coronary angiography. SIN-1 administration reduced cytosolic [Ca2+] in unstimulated platelets by decreasing Ca2+ influx. It attenuated Ca2+ mobilization from internal stores evoked by thrombin or thapsigargin. In vitro studies were used as an approach to investigate how simultaneous productions of NO and O2− from SIN-1 modify thrombin- or thapsigargin-induced platelet Ca2+ mobilization. Superoxide dismutase, the O2− scavenger, enhanced the capacity of SIN-1 to inhibit Ca2+ mobilization but catalase had no effect.This suggests that the effects of SIN-1 on platelet Ca2+ handling resemble those of NO, but are modulated by simultaneous O2− release, independently of H2O2 formation.

scholarly journals L-Arginine/Nitric Oxide Pathway and KCa Channels in Endothelial Cells: A Mini-Review

2020 ◽  
Author(s):  
Marcelo González ◽  
José Carlos Rivas
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Endothelial Function ◽  
Vascular Tone ◽  
Molecular Mechanisms ◽  
Cardiovascular Health ◽  
Kca Channels ◽  
Subsequent Activation ◽  
Regulation Of Vascular Tone

The endothelium is an organ with a key role in the maintenance of cardiovascular health through the regulation of vascular tone, vascular resistance, blood flow, and arterial pressure. These functions are related with the synthesis and release of vasoactive molecules, mainly vasodilators like nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). Both factors are released and diffused from endothelial cells to the smooth muscle cells, where there is a subsequent activation of signaling pathways that finally decrease the intracellular calcium to induce the vascular relaxation. The study of the molecular mechanisms that underlie the endothelial function still is in development, but from the evidence obtained from the endothelial cells in vitro studies are possible to partially describe the pathways to regulate the physiological endothelial function and the disturbances in pathological conditions. In this mini-review, we describe the main mechanisms for NO synthesis and the role of potassium channels related with EDHF. We include schemes and graphical summaries for better understanding of the molecular regulation of vascular tone in the human cardiovascular system.

Effect of Tumor Necrosis Factor-α on in vitro Prostaglandin Production in Buffalo Corpus Luteum

2021 ◽  
Author(s):  
M.K. Tripathi ◽  
S. Mondal ◽  
I.J. Reddy ◽  
A. Mor
Keyword(s):  
Mrna Expression ◽  
Corpus Luteum ◽  
Prostaglandin E ◽  
Prostaglandin F ◽  
Important Regulator ◽  
Factor Α ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Necrosis Factor

Background: Corpus luteum plays key role in embryonic survival. Prostaglandins are the important regulator controlling the life span of corpus luteum. The present study investigated the effect of various doses of TNFα on in vitro PGF2α and PGE2 production and expression profiling of PGFS and PGES mRNA in buffalo Corpus Luteum (CL).Methods: Buffalo ovaries with mid-luteal phase CL were collected from the abattoir and CL were enucleated from surrounding tissues. Corpus luteum were finely chopped, rinsed with HBSS (Hanks Balanced Salt Solution) medium; supplemented with gentamycin and 0.1% BSA and incubated at 37°C for 1 hr in HBSS containing 0.1% collagenase. The cell suspension following filtration was washed by HBBS supplemented with gentamycin and 0.1% BSA (bovine serum albumin) and was treated with increasing doses of TNFα (0.1, 0.5 and 1.0 nM) and cultured at 38.5°C, 5% CO2 level for 24 hr. Result: There was dose dependent increase in concentrations of PGF2α and PGE2 with increasing doses of TNFα. The PGFS (prostaglandin F synthase) mRNA expression increased with increasing doses of TNFα. However, there was decrease in PGES (prostaglandin E synthase) mRNA expression at 0.1 nM and 0.5 nM TNFα but PGES mRNA expression increased at 1.0 nM TNFα as compared to control. It can be concluded that TNFα may alter PGES and PGFS mRNA expression and prostaglandin secretion in buffalo CL. 

Chemical activation in Rhinella arenarum oocytes: effect of dehydroleucodine (DhL) and its hydrogenated derivative (2H-DhL)

Zygote ◽  
2014 ◽  
Vol 23 (6) ◽  
pp. 924-932
Author(s):  
M.F. Medina ◽  
M.I. Bühler ◽  
G. Sánchez-Toranzo
Keyword(s):  
Mechanism Of Action ◽  
Chemical Activation ◽  
Dependent Manner ◽  
Oocyte Activation ◽  
Parthenogenetic Activation ◽  
Intracellular Ca ◽  
Rhinella Arenarum ◽  
Dose Dependent ◽  
Maturation Promoting Factor

SummaryMature oocytes are arrested in metaphase II due to the presence of high levels of active maturation promoting factor (MPF). After fertilization, active MPF levels decline abruptly, enabling oocytes to complete meiosis II. One of the first and universal events of oocyte activation is an increase in cytosolic Ca2+ that would be responsible for MPF inactivation. Mature oocytes can also be activated by parthenogenetic activation. The aims of this work are to test the ability of dehydroleucodine (DhL) and its hydrogenated derivative 11,13-dihydro-dehydroleucodine (2H-DhL) to induce chemical activation in amphibian oocytes and to study the participation of calcium in the process. Results indicated that DhL and 2H-DhL induced oocyte activation in a dose-dependent manner. After 90 min of treatment, DhL 36 μM was able to induce 95% activation, while 2H-DhL 36 μM was less active, with only 40% activation. Our results suggest that DhL induced the inhibition of MPF activity, probably by an increase in intracellular Ca2+ concentration. Extracellular Ca2+ would not be significant, although Ca2+ release from intracellular stores is critical. In this sense, IP3Rs and RyRs were involved in the Ca2+ transient induced by lactones. In this species, RyRs appears to be the largest contributor to Ca2+ release in DhL-induced activation. Although more studies are needed on the mechanism of action through which these lactones induce oocyte activation in Rhinella arenarum, the results of this research provide interesting perspectives for the use of these lactones as chemical activators in in vitro fertilization and cloning.

15-HETE-substituted diglycerides selectively regulate PKC isotypes in human tracheal epithelial cells

1999 ◽  
Vol 277 (3) ◽  
pp. L457-L464 ◽  
Author(s):  
Stephen E. Alpert ◽  
Ronald W. Walenga ◽  
Atashi Mandal ◽  
Nicole Bourbon ◽  
Mark Kester
Keyword(s):  
High Performance ◽  
Neutral Lipids ◽  
Platelet Activating Factor ◽  
Dependent Manner ◽  
Western Blots ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial ◽  
Layer Chromatography ◽  
Dose Dependent

Human tracheal epithelial (TE) cells selectively incorporate their major lipoxygenase product, 15-hydroxyeicosatetraenoic acid (15-HETE), into the sn-2 position of phosphatidylinositol (PI) (S. E. Alpert and R. W. Walenga. Am. J. Respir. Cell Mol. Biol. 8: 273–281, 1993). Here we investigated whether 15-HETE-PI is a substrate for receptor-mediated generation of 15-HETE-substituted diglycerides (DGs) and whether these 15-HETE-DGs directly activate and/or alter conventional diacylglycerol-induced activation of protein kinase C (PKC) isotypes in these cells. Primary human TE monolayers incubated with 0.5 μM 15-[3H]-HETE or 15-[14C]HETE for 1–2 h were stimulated with 1 nM to 1 μM platelet-activating factor (PAF) for 30 s to 6 min, and the radiolabel in the medium, cellular phospholipids, and neutral lipids was assessed by high-performance liquid and thin-layer chromatography. PAF mobilized radiolabel from PI in a dose-dependent manner (22 ± 5% decrease after 1 μM PAF) without a concomitant release of free intra- or extracellular 15-HETE. 14C-labeled DGs were present in unstimulated TE monolayers incubated with 15-[14C]HETE, and the major 14C band, identified as sn-1,2-15-[14C]HETE-DG, increased transiently in response to PAF. Western blots of freshly isolated and cultured human TE cells revealed PKC isotypes α, βI, βII, δ, ε, and ζ. In vitro, cell-generated sn-1,2-15-[14C]HETE-DG selectively activated immunoprecipitated PKC-α and inhibited diacylglycerol-induced activation of PKC-α, -δ, -βI, and -βII. Our observations indicate that 15-HETE-DGs can modulate the activity of PKC isotypes in human TE cells and suggest an intracellular autocrine role for 15-HETE in human airway epithelia.

Comparative effects of the ionophore A23187 on the mechanical responses of muscle in normal Pietrain pigs and pigs with malignant hyperthermia

1986 ◽  
Vol 64 (3) ◽  
pp. 248-253 ◽  
Author(s):  
G. Reiss ◽  
G. Monin ◽  
C. Lauer
Keyword(s):  
Malignant Hyperthermia ◽  
Wide Spectrum ◽  
Human Subjects ◽  
Ionophore A23187 ◽  
Mechanical Responses ◽  
Intracellular Ca ◽  
Clear Differentiation ◽  
Dose Dependent ◽  
Muscle Biopsies

Since increased intracellular Ca2+ is believed to be the main factor causing skeletal muscle contracture in human and porcine malignant hyperthermia, the potential effects of the ionophore A23187, which enhances intracytoplasmic Ca2+, were investigated in Pietrain pig muscles. These effects were compared with those of caffeine, known to induce dose-dependent contracture in vitro in isolated muscle from human subjects with malignant hyperthermia. For this purpose, the mechanical and biochemical actions of caffeine and A23187 were tested in intercostal muscle biopsies from 10 normal pigs and 10 with malignant hyperthermia. The results show that A23187 allowed very clear differentiation between the muscles of normal and pathological animals. In view of the wide spectrum of drug sensitivity characterizing subjects with malignant hyperthermia, it is suggested that exposure to A23187 be added to the halothane and caffeine tests currently used to detect this disease.

scholarly journals Oral Administration of Glomerular Basement Membrane Prevents the Development of Experimental Autoimmune Glomerulonephritis in the WKY Rat

2001 ◽  
Vol 12 (1) ◽  
pp. 61-70
Author(s):  
JOHN REYNOLDS ◽  
CHARLES D. PUSEY
Keyword(s):  
T Cells ◽  
Basement Membrane ◽  
Oral Administration ◽  
Glomerular Basement Membrane ◽  
Crescent Formation ◽  
Necrotizing Glomerulonephritis ◽  
Wistar Kyoto ◽  
Dose Dependent ◽  
Experimental Autoimmune

Abstract. Experimental autoimmune glomerulonephritis (EAG), an animal model of Goodpasture's disease, can be induced in Wistar Kyoto (WKY) rats by a single injection of collagenase-solubilized rat glomerular basement membrane (GBM) in adjuvant. EAG is characterized by circulating and deposited anti-GBM antibodies, accompanied by focal necrotizing glomerulonephritis with crescent formation. The inhibitory effect of orally administered antigens has been reported in various animal models of autoimmunity but not in EAG in the rat. The effects of feeding rat GBM by gavage, at total doses of 0.5, 2.5, or 5 mg, before immunization were examined. A dose-dependent effect was observed on the development of EAG. A dose of 0.5 mg of GBM had no effect on disease, 2.5 mg resulted in a moderate reduction in the severity of nephritis but no change in anti-GBM antibody production, and 5 mg resulted in a marked reduction in circulating and deposited anti-GBM antibodies, albuminuria, deposits of fibrin in the glomeruli, severity of glomerular abnormalities, and numbers of infiltrating T cells and macrophages. Animals that were fed 5 mg of GBM showed a significant reduction in IgG2a but not IgG1, anti-GBM antibody levels, suggesting downregulation of Th1 responses. There was also a dose-dependent reduction in the proliferative responses of splenic T cells from treated animals to GBM antigen in vitro. These results clearly demonstrate that mucosal tolerance can be induced by oral administration of GBM antigen and that this approach is effective in preventing EAG.

ОСОБЕННОСТИ БИОФИЗИЧЕСКИХ СВОЙСТВ ФОРМЕННЫХ ЭЛЕМЕНТОВ КРОВИ ЛЮДЕЙ ПОЖИЛОГО ВОЗРАСТА В УСЛОВИЯХ МЕХАНИЧЕСКОГО СТРЕССА IN VITRO

2020 ◽  
Vol 65 (6) ◽  
pp. 1114-1117
Author(s):  
Е.А. Сладкова ◽  
◽  
М.Ю. Скоркина ◽  
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Vascular Tone ◽  
Tissue Oxygenation ◽  
Purinergic Receptor ◽  
The Elderly ◽  
Receptor Activation ◽  
Biophysical Properties ◽  
Regulation Of Vascular Tone

This study explores the peculiarities of biophysical properties in blood cells of the elderly under mechanical stress, applied in vitro, which, according to the literature data, triggers the signaling pathways engaged by purinergic receptor activation. Along with it, we detected a decrease in the stiffness of the cell surface of red blood cells, granulocytes, lymphocytes and platelets and the surface potential became more positive. Our findings could increase knowledge about the effect of mechanical deformation on leukocytes and platelets, which are the main regulators of homeostatic processes in the microvasculature, and on red blood cells involved in the regulation of vascular tone of arterioles and tissue oxygenation in the elderly.

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