Influence of Nifedipine on Functional Responses In Vivo Initiated at α2-Adrenoceptors

1983 ◽  
Vol 5 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Pieter B. M. W. M. Timmermans ◽  
Adriaan de Jonge ◽  
Jacques C. A. van Meel ◽  
Marie-Jeanne Mathy ◽  
Pieter A. van Zwieten
Keyword(s):  
Functional Responses ◽  
Α2 Adrenoceptors

scholarly journals Porcine small intestinal organoids as a model to explore ETEC–host interactions in the gut

2021 ◽  
Vol 52 (1) ◽  
Author(s):  
Bjarne Vermeire ◽  
Liara M. Gonzalez ◽  
Robert J. J. Jansens ◽  
Eric Cox ◽  
Bert Devriendt
Keyword(s):  
Intestinal Epithelial ◽  
Gut Health ◽  
Functional Responses ◽  
Host Pathogen Interactions ◽  
Epithelial Surface ◽  
Host Interactions ◽  
Intestinal Organoids ◽  
Host Pathogen ◽  
Small Intestinal

AbstractSmall intestinal organoids, or enteroids, represent a valuable model to study host–pathogen interactions at the intestinal epithelial surface. Much research has been done on murine and human enteroids, however only a handful studies evaluated the development of enteroids in other species. Porcine enteroid cultures have been described, but little is known about their functional responses to specific pathogens or their associated virulence factors. Here, we report that porcine enteroids respond in a similar manner as in vivo gut tissues to enterotoxins derived from enterotoxigenic Escherichia coli, an enteric pathogen causing postweaning diarrhoea in piglets. Upon enterotoxin stimulation, these enteroids not only display a dysregulated electrolyte and water balance as shown by their swelling, but also secrete inflammation markers. Porcine enteroids grown as a 2D-monolayer supported the adhesion of an F4+ ETEC strain. Hence, these enteroids closely mimic in vivo intestinal epithelial responses to gut pathogens and are a promising model to study host–pathogen interactions in the pig gut. Insights obtained with this model might accelerate the design of veterinary therapeutics aimed at improving gut health.

Cerebral haemodynamic response to somatosensory stimulation in preterm lambs and 7–10-day old lambs born at term: Direct synchrotron microangiography assessment

2021 ◽  
pp. 0271678X2110458
Author(s):  
Ishmael M Inocencio ◽  
Nhi T Tran ◽  
Shinji Nakamura ◽  
Song J Khor ◽  
Manon Wiersma ◽  
...  
Keyword(s):  
Near Infrared ◽  
Adult Brain ◽  
Haemodynamic Response ◽  
Functional Responses ◽  
Somatosensory Stimulation ◽  
Cerebral Microvessels ◽  
Microvascular Changes ◽  
Median Nerve Stimulation ◽  
Resolution Imaging

Neurovascular coupling has been well-defined in the adult brain, but variable and inconsistent responses have been observed in the neonatal brain. The mechanisms that underlie functional haemodynamic responses in the developing brain are unknown. Synchrotron radiation (SR) microangiography enables in vivo high-resolution imaging of the cerebral vasculature. We exploited SR microangiography to investigate the microvascular changes underlying the cerebral haemodynamic response in preterm (n = 7) and 7–10-day old term lambs (n = 4), following median nerve stimulation of 1.8, 4.8 and 7.8 sec durations. Increasing durations of somatosensory stimulation significantly increased the number of cortical microvessels of ≤200 µm diameter in 7–10-day old term lambs (p < 0.05) but not preterm lambs where, in contrast, stimulation increased the diameter of cerebral microvessels with a baseline diameter of ≤200 µm. Preterm lambs demonstrated positive functional responses with increased oxyhaemoglobin measured by near infrared spectroscopy, while 7–10-day old term lambs demonstrated both positive and negative responses. Our findings suggest the vascular mechanisms underlying the functional haemodynamic response differ between the preterm and 7–10-day old term brain. The preterm brain depends on vasodilatation of microvessels without recruitment of additional vessels, suggesting a limited capacity to mount higher cerebral haemodynamic responses when faced with prolonged or stronger neural stimulation.

scholarly journals Dicer1-mediated miRNA processing shapes the mRNA profile and function of murine platelets

Blood ◽  
2016 ◽  
Vol 127 (14) ◽  
pp. 1743-1751 ◽  
Author(s):  
Jesse W. Rowley ◽  
Stéphane Chappaz ◽  
Aurélie Corduan ◽  
Mark M. W. Chong ◽  
Robert Campbell ◽  
...  
Keyword(s):  
Functional Responses ◽  
Mirna Processing ◽  
Key Points ◽  
Mrna Profile ◽  
And Function

Key Points Dicer1 deletion in MKs alters platelet miRNA and mRNA profiles. Dicer1-deficient platelets display increased integrins αIIb and β3 levels and enhanced in vitro and in vivo functional responses.

scholarly journals Characterization of Prejunctional Muscarinic Receptors: Effects on the Release of VIP and Functional Responses and Receptor Expression in the Ovine Submandibular Gland

2009 ◽  
Vol 2009 ◽  
pp. 1-6
Author(s):  
Anders T. Ryberg ◽  
Ondrej Soukup ◽  
Gunnar Tobin
Keyword(s):  
Electrical Stimulation ◽  
Submandibular Gland ◽  
Muscarinic Receptor ◽  
Muscarinic Receptors ◽  
Receptor Expression ◽  
Receptor Subtypes ◽  
Chorda Tympani Nerve ◽  
Functional Responses ◽  
Stimulation Of

In the in vivo experiments on anaesthetized sheep, it was presently examined whether muscarinic receptor antagonists with diverse selectivity affect the release of VIP in response to electrical stimulation of the parasympathetic chorda tympanic nerve differently, and if the changes in the release could be associated to altered secretory and vasodilator responses. The location of the muscarinic receptor subtypes was examined also. In the experiments, blood was collected out of the submandibular venous drainage before and during electrical stimulation of chorda tympani nerve in the absence and presence either of pirenzepine or methoctramine. While metchoctramine increased the output of protein, pirenzepine inhibited flow of saliva and increased protein output, vasodilatation, and VIP output. In morphological examinations, the inhibitory muscarinic M4 receptor occurred interacinarily in the gland. It is concluded that prejunctional muscarinic receptors, most likely of the M4 subtype, exert inhibitory modulation of the parasympathetic release of VIP in the ovine submandibular gland.

Vascular responses in vivo to 8-epiPGF2α in normal and hypercholesterolemic pigs

2002 ◽  
Vol 283 (2) ◽  
pp. R303-R308 ◽  
Author(s):  
James D. Krier ◽  
Martin Rodriguez-Porcel ◽  
Patricia J. M. Best ◽  
J. Carlos Romero ◽  
Amir Lerman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Systemic Circulation ◽  
Renal Perfusion ◽  
High Dose ◽  
Functional Responses ◽  
Vascular Effects ◽  
Prostaglandin F ◽  
And Function ◽  
Single Kidney

Hypercholesterolemia (HC) is characterized by increased circulating 8- epi-prostaglandin-F2α (isoprostane), a vasoconstrictor, marker, and mediator of increased oxidative stress, whose vascular effects might be augmented in HC. Anesthetized pigs were studied in vivo with electron beam computed tomography after a 12-wk normal ( n = 8) or HC ( n = 8) diet. Mean arterial pressure (MAP), single-kidney perfusion, and glomerular filtration rate (GFR) were quantified before and during unilateral intrarenal infusions of U46619 (10 ng · kg−1 · min−1) or isoprostane (1 μg · kg−1 · min−1). Basal renal perfusion and function were similar, and isoprostane infusion elevated its systemic levels similarly in normal and HC (333 ± 89 vs. 366 ± 48 pg/ml, respectively, P < 0.01 vs. baseline). Both drugs markedly and comparably decreased cortical perfusion and GFR in both groups, whereas medullary perfusion decreased significantly only in HC. Moreover, MAP increased significantly only in HC (+9 ± 3 and +11 ± 3 mmHg, respectively, P≤ 0.05). Hence, in HC, renal functional responses to high-dose isoprostane are largely similar to normal, but the systemic circulation exhibits augmented sensitivity to pathophysiological levels of isoprostane and U46619 , which may potentially play a role in development of hypertension and vascular injury associated with increased oxidative stress.

scholarly journals The effect of in vitro exposure to antisense oligonucleotides on macrophage morphology and function

2011 ◽  
Vol 2 (1) ◽  
pp. 12 ◽  
Author(s):  
Ann Brasey ◽  
Raouf Igue ◽  
Loubna Djemame ◽  
Serge Séguin ◽  
Paolo Renzi ◽  
...  
Keyword(s):  
Antisense Oligonucleotides ◽  
Morphological Changes ◽  
Lower Airway ◽  
Functional Responses ◽  
Phagocytic Capacity ◽  
Proinflammatory Mediators ◽  
Functional Consequences ◽  
And Function

<p>Antisense oligonucleotides (AON) delivered via inhalation are in drug development for respiratory diseases. In rodents and monkeys, repeated exposure to high doses of inhaled phosphorothioate (PS) AON can lead to microscopic changes in the lungs, including accumulation of alveolar macrophages in the lower airway that have a <em>foamy</em> appearance. The functional consequences that result from this morphological change are unclear as there is controversy whether the vacuoles/inclusion bodies reflect normal clearance of the inhaled AON or are early indicators of lung toxicity. The morphological and functional responses of macrophage to PS AON were characterized <em>in vitro</em> using the comparator drug amiodarone, as a known inducer of foamy macrophages. Morphological changes of increased vacuolization with the presence of lamellated structures were observed in macrophages in response to both amiodarone and AON treatment. Functional responses to the drugs clearly differed with amiodarone treatment leading to apoptosis of cells and cell death, release of proinflammatory mediators IL-1RA, MIP-1<em>α </em>and TNF<em>α</em>, decrease in IP-10, a cytokine shown to be involved in protection against pulmonary fibrosis and altered phagocytosis capacity of the cells. In contrast, AON in concentrations up to 30 μM, had no effect on cell viability or apoptosis, had minimal effects on pro-inflammatory cytokines, increased IP-10 levels and did not alter the phagocytic capacity of the cells. Exposure of macrophages to AON<em> in vitro</em>, led to morphological changes of increased vacuolization, but did not lead to functional consequences which were observed with another vacuolization-inducing drug, suggesting that the <em>in vivo </em>phenotypic changes observed following inhalation of AON may be consistent with a clearance mechanism and not an activation or impairment of macrophages.</p>

Altered biomechanical properties of carotid arteries in two mouse models of muscular dystrophy

2007 ◽  
Vol 103 (2) ◽  
pp. 664-672 ◽  
Author(s):  
W. W. Dye ◽  
R. L. Gleason ◽  
E. Wilson ◽  
J. D. Humphrey
Keyword(s):  
Muscular Dystrophy ◽  
Axial Force ◽  
Carotid Arteries ◽  
Structural Integrity ◽  
Muscle Cells ◽  
Biomechanical Properties ◽  
Axial Stiffness ◽  
Wild Type ◽  
Functional Responses

Muscular dystrophy is characterized by skeletal muscle weakness and wasting, but little is known about possible alterations to the vasculature. Many muscular dystrophies are caused by a defective dystrophin-glycoprotein complex (DGC), which plays an important role in mechanotransduction and maintenance of structural integrity in muscle cells. The DGC is a group of membrane-associated proteins, including dystrophin and sarcoglycan-δ, that helps connect the cytoskeleton of muscle cells to the extracellular matrix. In this paper, mice lacking genes encoding dystrophin ( mdx) or sarcoglycan-δ ( sgcd−/−) were studied to detect possible alterations to vascular wall mechanics. Pressure-diameter and axial force-length tests were performed on common carotid arteries from mdx, sgcd−/−, and wild-type mice in active (basal) and passive smooth muscle states, and functional responses to three vasoactive compounds were determined at constant pressure and length. Apparent biomechanical differences included the following: mdx and sgcd−/− arteries had decreased distensibilities in pressure-diameter tests, with mdx arteries exhibiting elevated circumferential stresses, and mdx and sgcd−/− arteries generated elevated axial loads and stresses in axial force-length tests. Interestingly, however, mdx and sgcd−/− arteries also had significantly lower in vivo axial stretches than did the wild type. Accounting for this possible adaptation largely eliminated the apparent differences in circumferential and axial stiffness, thus suggesting that loss of DGC proteins may induce adaptive biomechanical changes that can maintain overall wall mechanics in response to normal loads. Nevertheless, there remains a need to understand better possible vascular adaptations in response to sustained altered loads in patients with muscular dystrophy.

scholarly journals Critical role of phospholipase Cγ2 in integrin and Fc receptor-mediated neutrophil functions and the effector phase of autoimmune arthritis

2009 ◽  
Vol 206 (3) ◽  
pp. 577-593 ◽  
Author(s):  
Zoltán Jakus ◽  
Edina Simon ◽  
David Frommhold ◽  
Markus Sperandio ◽  
Attila Mócsai
Keyword(s):  
Critical Role ◽  
Fc Receptor ◽  
Src Family Kinases ◽  
Autoimmune Arthritis ◽  
Functional Responses ◽  
Fcγ Receptors ◽  
Effector Phase ◽  
Β2 Integrins

β2 integrins and Fcγ receptors are critically involved in neutrophil activation at the site of inflammation. Both receptor types trigger a receptor-proximal tyrosine phosphorylation cascade through Src family kinases and Syk, but further downstream signaling events are poorly understood. We show that phospholipase C (PLC) γ2 is phosphorylated downstream of Src family kinases and Syk during integrin or Fc receptor-mediated activation of neutrophils. PLCγ2−/− neutrophils are completely defective in β2 integrin or Fcγ receptor-mediated functional responses such as respiratory burst, degranulation, or cell spreading in vitro and show reduced adhesion/spreading in inflamed capillary venules in vivo. However, PLCγ2−/− neutrophils respond normally to various other agonists, including chemokines, bacterial formyl peptides, Toll-like receptor ligands, or proinflammatory cytokines, and migrate normally both in vitro and in vivo. To confirm the in vivo relevance of these observations, the effect of the PLCγ2−/− mutation was tested in the K/B×N serum transfer arthritis model, which is known to require β2 integrins, Fcγ receptors, and neutrophils. PLCγ2 deficiency completely protected mice from clinical signs and histological features of arthritis as well as from arthritis-induced loss of articular function. These results identify PLCγ2 as a critical player of integrin and Fc receptor-mediated neutrophil functions and the neutrophil-mediated effector phase of autoimmune arthritis.

Does rilmenidine act in vivo on central α2-adrenoceptors modulating noradrenaline release?

1992 ◽  
Vol 213 (2) ◽  
pp. 305-307 ◽  
Author(s):  
M.F. Suaud-Chagny ◽  
C. Mermet ◽  
E. Tibiriça ◽  
P. Bousquet ◽  
F. Gonon
Keyword(s):  
Noradrenaline Release ◽  
Α2 Adrenoceptors
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