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Journal articles on the topic 'Contractilité vasculaire'

Author: Grafiati

Published: 4 June 2021

Last updated: 14 February 2022

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1

Rhoades, R. A., C. S. Packer, and R. A. Meiss. "Pulmonary Vascular Smooth Muscle Contractility." Chest 93, no. 3 (1988): 94S—95S. http://dx.doi.org/10.1378/chest.93.3_supplement.94s.

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2

Ogoh, Shigehiko, Gilbert Moralez, Takuro Washio, et al. "Effect of increases in cardiac contractility on cerebral blood flow in humans." American Journal of Physiology-Heart and Circulatory Physiology 313, no. 6 (2017): H1155—H1161. http://dx.doi.org/10.1152/ajpheart.00287.2017.

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The effect of acute increases in cardiac contractility on cerebral blood flow (CBF) remains unknown. We hypothesized that the external carotid artery (ECA) downstream vasculature modifies the direct influence of acute increases in heart rate and cardiac function on CBF regulation. Twelve healthy subjects received two infusions of dobutamine [first a low dose (5 μg·kg−1·min−1) and then a high dose (15 μg·kg−1·min−1)] for 12 min each. Cardiac output, blood flow through the internal carotid artery (ICA) and ECA, and echocardiographic measurements were performed during dobutamine infusions. Despit

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3

Barrese, Vincenzo, Jennifer B. Stott, Samuel N. Baldwin, Gema Mondejar-Parreño, and Iain A. Greenwood. "SMIT (Sodium-Myo-Inositol Transporter) 1 Regulates Arterial Contractility Through the Modulation of Vascular Kv7 Channels." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 10 (2020): 2468–80. http://dx.doi.org/10.1161/atvbaha.120.315096.

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Objective: The SMIT1 (sodium:myo-inositol transporter 1) regulates myo-inositol movement into cells and responses to hypertonic stimuli. Alteration of myo-inositol levels has been associated with several diseases, including hypertension, but there is no evidence of a functional role of SMIT1 in the vasculature. Recent evidence showed that in the nervous system SMIT1 interacted and modulated the function of members of the Kv7 family of voltage-gated potassium channels, which are also expressed in the vasculature where they regulate arterial contractility. Therefore, in this study, we evaluated

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4

Chen, Li, Bin Zhang, Lu Yang, et al. "BMAL1 Disrupted Intrinsic Diurnal Oscillation in Rat Cerebrovascular Contractility of Simulated Microgravity Rats by Altering Circadian Regulation of miR-103/CaV1.2 Signal Pathway." International Journal of Molecular Sciences 20, no. 16 (2019): 3947. http://dx.doi.org/10.3390/ijms20163947.

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The functional and structural adaptations in cerebral arteries could be one of the fundamental causes in the occurrence of orthostatic intolerance after space flight. In addition, emerging studies have found that many cardiovascular functions exhibit circadian rhythm. Several lines of evidence suggest that space flight might increase an astronaut’s cardiovascular risks by disrupting circadian rhythm. However, it remains unknown whether microgravity disrupts the diurnal variation in vascular contractility and whether microgravity impacts on circadian clock system. Sprague-Dawley rats were subje

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5

Legan, Eugenia, Bryan Roth, Toshio Nakaki, De Chuang, Joseph Parrilló, and Bart Chernow. "REGULATION OF NOREPINEPHRINE-MEDIATED VASCULAR CONTRACTILITY." Critical Care Medicine 13, no. 4 (1985): 278. http://dx.doi.org/10.1097/00003246-198504000-00041.

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6

Li, S., S. X. Fan, and T. M. McKenna. "Vascular smooth muscle cells on Matrigel as a model for LPS-induced hypocontractility and NO formation." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 1 (1997): H576—H584. http://dx.doi.org/10.1152/ajpheart.1997.272.1.h576.

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Treatment of vascular tissue with low levels of lipopolysaccharide (LPS) induces nitric oxide synthase (NOS) activity and diminishes vascular contractility. However, in cultured vascular smooth muscle cells (VSMC), very high doses of LPS or the combination of LPS with cytokines are required for the induction of nitric oxide (NO) formation. The aims of this study were to establish a cell model to investigate LPS-induced hypocontractility and NO production and to test the hypothesis that responses of VSMC to LPS are differentiation regulated. We used Matrigel basement membrane matrix to maintain

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7

Faulkner, Jessica L., Daisy Harwood, Simone Kennard, Galina Antonova, Nicolas Clere, and Eric J. Belin de Chantemèle. "Dietary sodium restriction sex specifically impairs endothelial function via mineralocorticoid receptor-dependent reduction in NO bioavailability in Balb/C mice." American Journal of Physiology-Heart and Circulatory Physiology 320, no. 1 (2021): H211—H220. http://dx.doi.org/10.1152/ajpheart.00413.2020.

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Female sex confers improved endothelial relaxation and vascular constriction responses in female Balb/C mice compared with males under baseline conditions. Sodium restriction impairs endothelial function, which is nitric oxide dependent, and increases vascular contractility in association with reduced vascular endothelial nitric oxide synthase and NOX4 expression in female mice ablating the baseline sex difference. Mineralocorticoid receptor antagonism ablates sodium restriction-induced endothelial dysfunction, but not increased vascular contractility, in female mice.

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8

Sorensen, Dane W., Desirelys Carreon, James M. Williams, and William J. Pearce. "Hypoxic modulation of fetal vascular MLCK abundance, localization, and function." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 320, no. 1 (2021): R1—R18. http://dx.doi.org/10.1152/ajpregu.00212.2020.

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Changes in vascular contractility are among the most important physiological effects of acute and chronic fetal hypoxia. Given the essential role of myosin light-chain kinase (MLCK) in smooth muscle contractility and its heterogeneous distribution, this study explores the hypothesis that subcellular changes in MLCK distribution contribute to hypoxic modulation of fetal carotid artery contractility. Relative to common carotid arteries from normoxic term fetal lambs (FN), carotids from fetal lambs gestated at high altitude (3,802 m) (FH) exhibited depressed contractility without changes in MLCK

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9

Mano, Mark T., Sotiria Bexis, Mahinda Y. Abeywardena, et al. "Fish Oils Modulate Blood Pressure and Vascular Contractility in the Rat and Vascular Contractility in the Primate." Blood Pressure 4, no. 3 (1995): 177–86. http://dx.doi.org/10.3109/08037059509077591.

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10

Philip, Jennifer L., Thomas M. Murphy, David A. Schreier, et al. "Pulmonary vascular mechanical consequences of ischemic heart failure and implications for right ventricular function." American Journal of Physiology-Heart and Circulatory Physiology 316, no. 5 (2019): H1167—H1177. http://dx.doi.org/10.1152/ajpheart.00319.2018.

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Left heart failure (LHF) is the most common cause of pulmonary hypertension, which confers an increase in morbidity and mortality in this context. Pulmonary vascular resistance has prognostic value in LHF, but otherwise the mechanical consequences of LHF for the pulmonary vasculature and right ventricle (RV) remain unknown. We sought to investigate mechanical mechanisms of pulmonary vascular and RV dysfunction in a rodent model of LHF to address the knowledge gaps in understanding disease pathophysiology. LHF was created using a left anterior descending artery ligation to cause myocardial infa

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11

Je, Hyun-Dong, Cynthia Gallant, Paul C. Leavis, and Kathleen G. Morgan. "Caveolin-1 regulates contractility in differentiated vascular smooth muscle." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 1 (2004): H91—H98. http://dx.doi.org/10.1152/ajpheart.00472.2003.

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Caveolin is a principal component of caveolar membranes. In the present study, we utilized a decoy peptide approach to define the degree of involvement of caveolin in PKC-dependent regulation of contractility of differentiated vascular smooth muscle. The primary isoform of caveolin in ferret aorta vascular smooth muscle is caveolin-1. Chemical loading of contractile vascular smooth muscle tissue with a synthetic caveolin-1 scaffolding domain peptide inhibited PKC-dependent increases in contractility induced by a phorbol ester or an α agonist. Peptide loading also resulted in a significant inhi

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12

Khayyal, M. A., C. Eng, D. Franzen, J. A. Breall, and E. S. Kirk. "Effects of vasopressin on the coronary circulation: reserve and regulation during ischemia." American Journal of Physiology-Heart and Circulatory Physiology 248, no. 4 (1985): H516—H522. http://dx.doi.org/10.1152/ajpheart.1985.248.4.h516.

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In 18 dogs, intracoronary infusion of vasopressin produced a 40% reduction in coronary flow without significantly affecting systemic hemodynamics. The blood flow reduction occurred in a uniform transmural pattern without evidence of a gradient. The reduction in coronary flow resulted in a decrease in regional contractility as determined by isometric strain gauge arches. The decrease in regional contractility was transiently reversed by bolus injection of adenosine into the perfusion line. This suggests that the reduction of blood flow due to vasopressin was causing ischemia. Evidence for ische

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13

Lee, Young Ho, Jeong Hwan Seo, and Bok Soon Kang. "Effects of hypoxia on pulmonary vascular contractility." Yonsei Medical Journal 39, no. 3 (1998): 261. http://dx.doi.org/10.3349/ymj.1998.39.3.261.

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14

Vedernikov, Yuri, Ancizar Betancourt, George Saade, and Robert Garfield. "Oxytocin controls uterine vascular contractility during pregnancy." American Journal of Obstetrics and Gynecology 189, no. 6 (2003): S187. http://dx.doi.org/10.1016/j.ajog.2003.10.470.

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15

Purdy, R. E., S. P. Duckles, D. N. Krause, K. M. Rubera, and D. Sara. "Effect of simulated microgravity on vascular contractility." Journal of Applied Physiology 85, no. 4 (1998): 1307–15. http://dx.doi.org/10.1152/jappl.1998.85.4.1307.

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Microgravity was simulated in Sprague-Dawley (SD) and Wistar (W) rats by using a tail harness to elevate the hindquarters, producing hindlimb unweighting (HU). After 20 days of HU treatment, blood vessels from both HU and control rats were cut into 3-mm rings and mounted in tissue baths for the measurement of isometric contraction. HU treatment decreased the contractile response to 68 mM K+ in abdominal aorta from W rats. HU treatment also decreased the contraction to 68 mM K+ in carotid arteries from both rat strains and in femoral arteries from W but not SD rats. HU treatment reduced the max

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16

Bergler, Tobias, Markus Resch, Stephan W. Reinhold, et al. "Cyclosporine A Impairs Norepinephrine-Induced Vascular Contractility." Kidney and Blood Pressure Research 35, no. 6 (2012): 655–62. http://dx.doi.org/10.1159/000342591.

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17

Nosaka, S., H. Kamaya, and K. C. Wong. "LOCAL ANESTHETIC TOXICITY ON VASCULAR MUSCLE CONTRACTILITY." Anesthesia & Analgesia 67, Supplement (1988): 158. http://dx.doi.org/10.1213/00000539-198802001-00158.

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18

Ubeda, M., F. Fenoy, L. F. Carbonell, et al. "Effect of captopril on norepinephrine vascular contractility." General Pharmacology: The Vascular System 16, no. 3 (1985): 303–6. http://dx.doi.org/10.1016/0306-3623(85)90091-6.

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19

Johns, Anthony, Paul Leijten, Hiro Yamamoto, Kwang Hwang, and Cornelis van Breemen. "Calcium regulation in vascular smooth muscle contractility." American Journal of Cardiology 59, no. 2 (1987): A18—A23. http://dx.doi.org/10.1016/0002-9149(87)90171-8.

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20

Gelman, Simon. "Classic Papers Revisited: My Love Affair with the Venous System." Anesthesiology 129, no. 2 (2018): 329–32. http://dx.doi.org/10.1097/aln.0000000000002280.

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Abstract The Pathophysiology of Aortic Cross-clamping and Unclamping. By Gelman S. ANesthesiology 1995; 82:1026–60. Reprinted with permission. Aortic cross-clamping (AoX) and unclamping are associated with severe hemodynamic disturbances in virtually all organs and systems. The main hemodynamic changes induced by AoX result from an increase in impedance to aortic flow, an increase in systemic vascular resistance and afterload, blood volume redistribution caused by collapse and constriction of venous vasculature distal to the aortic clamp, and a subsequent increase in preload. Preload may not i

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21

Kolumam Parameswaran, Praveen, Daying Dai, Yong-Hong Ding, et al. "Downstream vascular changes after flow-diverting device deployment in a rabbit model." Journal of NeuroInterventional Surgery 11, no. 5 (2018): 523–27. http://dx.doi.org/10.1136/neurintsurg-2018-014123.

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BackgroundFlow diverters (FDs) are increasingly used in the treatment of intracranial aneurysms, and carry the risk of thromboembolic complications, even in patients treated with dual antiplatelet therapy. The effect of FDs on the downstream vascular is unknown. The aim of the study was to investigate vascular wall pulse wave velocity (PWV) and contractility changes following FD treatment in a rabbit model.MethodsFDs (Pipeline Embolic Device, Medtronic Inc., Irvine, California, USA) were implanted in the aorta of normal rabbits and sham-operated aorta were used as controls (n=6 per group). Pul

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22

Westerhof, Nico, Christa Boer, Regis R. Lamberts, and Pieter Sipkema. "Cross-Talk Between Cardiac Muscle and Coronary Vasculature." Physiological Reviews 86, no. 4 (2006): 1263–308. http://dx.doi.org/10.1152/physrev.00029.2005.

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The cardiac muscle and the coronary vasculature are in close proximity to each other, and a two-way interaction, called cross-talk, exists. Here we focus on the mechanical aspects of cross-talk including the role of the extracellular matrix. Cardiac muscle affects the coronary vasculature. In diastole, the effect of the cardiac muscle on the coronary vasculature depends on the (changes in) muscle length but appears to be small. In systole, coronary artery inflow is impeded, or even reversed, and venous outflow is augmented. These systolic effects are explained by two mechanisms. The waterfall

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23

Peroni, Roxana N., Tamara Abramoff, Isabel Neuman, Ernesto J. Podestá, and Edda Adler-Graschinsky. "Phytoestrogens Enhance the Vascular Actions of the Endocannabinoid Anandamide in Mesenteric Beds of Female Rats." International Journal of Hypertension 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/647856.

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In rat isolated mesenteric beds that were contracted with NA as an in vitro model of the vascular adrenergic hyperactivity that usually precedes the onset of primary hypertension, the oral administration (3 daily doses) of either 10 mg/kg genistein or 20 mg/kg daidzein potentiated the anandamide-induced reduction of contractility to NA in female but not in male rats. Oral treatment with phytoestrogens also restored the vascular effects of anandamide as well as the mesenteric content of calcitonin gene-related peptide (CGRP) that were reduced after ovariectomy. The enhancement of anandamide eff

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24

Leszczynska, Katarzyna, Sukhbir Kaur, Eleanor Wilson, Roy Bicknell, and Victoria L. Heath. "The role of RhoJ in endothelial cell biology and angiogenesis." Biochemical Society Transactions 39, no. 6 (2011): 1606–11. http://dx.doi.org/10.1042/bst20110702.

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RhoJ is an endothelially expressed member of the Cdc42 (cell division cycle 42) subfamily of small Rho GTPases. It is expressed in both the developing mammalian vasculature and the vascular beds of a number of adult tissues, with its expression regulated by the endothelial transcription factor ERG (ETS-related gene). RhoJ has been shown to regulate endothelial motility, tubulogenesis and lumen formation in vitro, and modulates the vascularization of Matrigel plugs in vivo. Both vascular endothelial growth factor and semaphorin 3E have been found to affect its activation. RhoJ has been shown to

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25

Liu, De-Jun, Wei Chen, Yan-Miao Huo, et al. "Prostacyclin decreases splanchnic vascular contractility in cirrhotic rats." Hepatobiliary & Pancreatic Diseases International 13, no. 4 (2014): 416–22. http://dx.doi.org/10.1016/s1499-3872(14)60270-8.

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26

Nishimura, T., E. Tatsumi, T. Nishinaka, Y. Taenaka, M. Nakata, and H. Takano. "Prolonged Nonpulsatile Left Heart Bypass Diminishes Vascular Contractility." International Journal of Artificial Organs 22, no. 7 (1999): 492–98. http://dx.doi.org/10.1177/039139889902200707.

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27

Dietrich, Alexander, Michael Mederos y Schnitzler, Maik Gollasch, et al. "Increased Vascular Smooth Muscle Contractility in TRPC6−/− Mice." Molecular and Cellular Biology 25, no. 16 (2005): 6980–89. http://dx.doi.org/10.1128/mcb.25.16.6980-6989.2005.

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ABSTRACT Among the TRPC subfamily of TRP (classical transient receptor potential) channels, TRPC3, -6, and -7 are gated by signal transduction pathways that activate C-type phospholipases as well as by direct exposure to diacylglycerols. Since TRPC6 is highly expressed in pulmonary and vascular smooth muscle cells, it represents a likely molecular candidate for receptor-operated cation entry. To define the physiological role of TRPC6, we have developed a TRPC6-deficient mouse model. These mice showed an elevated blood pressure and enhanced agonist-induced contractility of isolated aortic rings

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Dietrich, Alexander, Michael Mederos y Schnitzler, Maik Gollasch, et al. "Increased Vascular Smooth Muscle Contractility in TRPC6−/− Mice." Molecular and Cellular Biology 25, no. 24 (2005): 11191. http://dx.doi.org/10.1128/mcb.25.24.11191.2005.

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29

Maze, M., P. Prokocimer, C. K. Spiss, D. M. Gaba, G. Tsujiraoto, and B. B. Hoffman. "ADRENERGIC HYPORESPONSIVENESS OF VASCULAR CONTRACTILITY FOLLOWING EPINEPHRINE INFUSION." Anesthesiology 63, Supplement (1985): A116. http://dx.doi.org/10.1097/00000542-198509001-00116.

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30

Alford, Patrick W., Alexander P. Nesmith, Johannes N. Seywerd, Anna Grosberg, and Kevin Kit Parker. "Vascular smooth muscle contractility depends on cell shape." Integrative Biology 3, no. 11 (2011): 1063–70. http://dx.doi.org/10.1039/c1ib00061f.

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31

Kida, Taiki, Kei Sawada, Koji Kobayashi, Masatoshi Hori, Hiroshi Ozaki, and Takahisa Murata. "Diverse effects of prostaglandin E2 on vascular contractility." Heart and Vessels 29, no. 3 (2013): 390–95. http://dx.doi.org/10.1007/s00380-013-0374-6.

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32

Nassar, Taher, Khalil Bdeir, Serge Yarovoi, et al. "tPA regulates pulmonary vascular activity through NMDA receptors." American Journal of Physiology-Lung Cellular and Molecular Physiology 301, no. 3 (2011): L307—L314. http://dx.doi.org/10.1152/ajplung.00429.2010.

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Tissue-type plasminogen activator (tPA) is a potent fibrinolytic enzyme used to treat acute coronary artery obstruction. However, tPA has shown limited utility in other disorders caused by thrombotic vascular occlusion, such as pulmonary embolism. We found that tPA caused dose-dependent effects on the contractility of pulmonary arterial rings that may affect its effectiveness as a thrombolytic agent. At low concentrations (1 nM), tPA stimulated pulmonary vascular contraction in response to phenylephrine, whereas at higher concentrations (20 nM) tPA inhibited pulmonary arterial contractility an

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33

Short, Ben. "The CCM complex puts a cap on integrin activity." Journal of Cell Biology 202, no. 3 (2013): 399. http://dx.doi.org/10.1083/jcb.2023if.

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34

Wehbe, Nadine, Suzanne Awni Nasser, Yusra Al-Dhaheri, et al. "EPAC in Vascular Smooth Muscle Cells." International Journal of Molecular Sciences 21, no. 14 (2020): 5160. http://dx.doi.org/10.3390/ijms21145160.

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Vascular smooth muscle cells (VSMCs) are major components of blood vessels. They regulate physiological functions, such as vascular tone and blood flow. Under pathological conditions, VSMCs undergo a remodeling process known as phenotypic switching. During this process, VSMCs lose their contractility and acquire a synthetic phenotype, where they over-proliferate and migrate from the tunica media to the tunica interna, contributing to the occlusion of blood vessels. Since their discovery as effector proteins of cyclic adenosine 3′,5′-monophosphate (cAMP), exchange proteins activated by cAMP (EP

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35

Coutsos, Matthew, Javier A. Sala-Mercado, Masashi Ichinose, ZhenHua Li, Elizabeth J. Dawe, and Donal S. O'Leary. "Muscle metaboreflex-induced coronary vasoconstriction limits ventricular contractility during dynamic exercise in heart failure." American Journal of Physiology-Heart and Circulatory Physiology 304, no. 7 (2013): H1029—H1037. http://dx.doi.org/10.1152/ajpheart.00879.2012.

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Muscle metaboreflex activation (MMA) during dynamic exercise increases cardiac work and myocardial O2 demand via increases in heart rate, ventricular contractility, and afterload. This increase in cardiac work should lead to metabolic coronary vasodilation; however, no change in coronary vascular conductance occurs. This indicates that the MMA-induced increase in sympathetic activity to the heart, which raises heart rate, ventricular contractility, and cardiac output, also elicits coronary vasoconstriction. In heart failure, cardiac output does not increase with MMA presumably due to impaired

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36

Yamawaki, Hideyuki. "Vascular Effects of Novel Adipocytokines: Focus on Vascular Contractility and Inflammatory Responses." Biological & Pharmaceutical Bulletin 34, no. 3 (2011): 307–10. http://dx.doi.org/10.1248/bpb.34.307.

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37

Saito, Toshiro. "The vascular clock system generates the intrinsic circadian rhythm of vascular contractility." Journal of Smooth Muscle Research 51 (2015): 95–106. http://dx.doi.org/10.1540/jsmr.51.95.

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38

Joe, Bina, Cameron G. McCarthy, Jonnelle M. Edwards, et al. "Microbiota Introduced to Germ-Free Rats Restores Vascular Contractility and Blood Pressure." Hypertension 76, no. 6 (2020): 1847–55. http://dx.doi.org/10.1161/hypertensionaha.120.15939.

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Commensal gut microbiota are strongly correlated with host hemodynamic homeostasis but only broadly associated with cardiovascular health. This includes a general correspondence of quantitative and qualitative shifts in intestinal microbial communities found in hypertensive rat models and human patients. However, the mechanisms by which gut microbes contribute to the function of organs important for blood pressure (BP) control remain unanswered. To examine the direct effects of microbiota on BP, we conventionalized germ-free (GF) rats with specific pathogen-free rats for a short-term period of

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Wang, Yujia, Zenghui Wu, Eric Thorin, et al. "Estrogen and testosterone in concert with EFNB3 regulate vascular smooth muscle cell contractility and blood pressure." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 7 (2016): H861—H872. http://dx.doi.org/10.1152/ajpheart.00873.2015.

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EPH kinases and their ligands, ephrins (EFNs), have vital and diverse biological functions, although their function in blood pressure (BP) control has not been studied in detail. In the present study, we report that Efnb3 gene knockout (KO) led to increased BP in female but not male mice. Vascular smooth muscle cells (VSMCs) were target cells for EFNB3 function in BP regulation. The deletion of EFNB3 augmented contractility of VSMCs from female but not male KO mice, compared with their wild-type (WT) counterparts. Estrogen augmented VSMC contractility while testosterone reduced it in the absen

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40

Schmidt, Christoph, Carl Roosens, Michel Struys, et al. "Contractility in Humans after Coronary Artery Surgery." Anesthesiology 91, no. 1 (1999): 58–70. http://dx.doi.org/10.1097/00000542-199907000-00012.

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Background Propofol's unique pharmacokinetic profile offers advantages for titration and rapid emergence in patients after coronary artery bypass graft (CABG) surgery, but concern for negative inotropic properties potentially limits its use in these patients. The current study analyzed the effect of various propofol plasma concentrations on left ventricular (LV) contractility by means of a single-beat contractile index based on LV maximal power (PWR(max)). Methods The study was conducted in 30 patients after CABG surgery. Immediately after admission to the intensive care unit (ICU), four diffe

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Gao, Ge, Jing-Jing Li, Yuenan Li, et al. "Rapamycin inhibits hydrogen peroxide-induced loss of vascular contractility." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 5 (2011): H1583—H1594. http://dx.doi.org/10.1152/ajpheart.01084.2010.

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Rapamycin, an inhibitor of the mammalian target of rapamycin (mTOR) pathway, has been shown to extend the life span of mice, and oxidative stress plays critical roles in vascular aging involving loss of compliance of arteries. We examined, therefore, whether rapamycin has protective effects on the inhibition of vascular contractility by hydrogen peroxide (H2O2). Prolonged (3 h) exposure to H2O2 induced complete loss of contraction of mouse aortic rings and mesenteric (resistance) arteries to either KCl or phenylephrine, which was attenuated by pretreatment with rapamycin. H2O2-induced loss of

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42

Arribas, Silvia M., Rosa Costa, Salvatore Salomone, Nicole Morel, Theophile Godfraind, and John C. McGrath. "Functional Reduction and Associated Cellular Rearrangement in SHRSP Rat Basilar Arteries Are Affected by Salt Load and Calcium Antagonist Treatment." Journal of Cerebral Blood Flow & Metabolism 19, no. 5 (1999): 517–27. http://dx.doi.org/10.1097/00004647-199905000-00006.

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The stroke-prone spontaneously hypertensive rat (SHRSP) is a strain with high incidence of cerebrovascular accidents increased by salt-rich diet and decreased by calcium-antagonist treatment. In the SHRSP rat basilar artery the authors have previously shown reduced contractility and altered structure including regions of smooth muscle cell (SMC) disorganization, The aims of this study have been to analyze (I) the morphology of these abnormal regions, (2) the structural modifications responsible for the reduced function, and (3) the effect of salt and calcium-antagonist treatment on vascular st

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Amin, Hesham M., Marco Cigada, Tawfic S. Hakim, and Enrico M. Camporesi. "Pulmonary mechanical and vascular responses after acute hyperbaric oxygen exposure." Canadian Journal of Physiology and Pharmacology 71, no. 8 (1993): 592–96. http://dx.doi.org/10.1139/y93-083.

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Pulmonary mechanical and vascular responses were studied in Sprague–Dawley rats exposed to hyperbaric oxygen (HBO, 100% O2 at 2.8 atm (1 atm = 101.325 kPa) for 6 h). Two groups of animals were examined after HBO exposure: group HBO comprised rats examined immediately after exposure and group R consisted of rats left recovering while breathing air for 24 h before being studied. Both groups were compared with control rats, group C, not exposed to HBO. Pulmonary mechanical responses were measured by quantitating static lung compliance (Cs), wet to dry weight ratio (W/D) of lung tissue, and surfac

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Dimitrova, Daniela, Biliana Nikolova, Vanya Bogoeva, et al. "Do Mistletoe (Viscum album L.) Lectins Influence Isometric Contraction of Non-diseased Human Mesenteric Arteries ex vivo?" International Journal Bioautomation 25, no. 1 (2021): 41–52. http://dx.doi.org/10.7546/ijba.2021.25.1.000788.

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Mistletoe (Viscum album L., VA) lectins (MLs) are plant lectins with potent anticancer activity. Although wide use of VA extracts in curing cancer, the effects of purified MLs on human vasculature in term of possible side effect of the lectin has not yet been reported. The present study was aimed to investigate isometric contractions of isolated human mesenteric arteries during MLs application. The contractile response of arteries was studied using Mulvany-Halpern myograph and the isometric contractions under MLs’ treatment were examined in artery segments with either intact endothelium or aft

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Woolfson, Robin G., Nicholas T. Richards, and Lucilla Poston. "Low-concentration ouabain does not inhibit noradrenaline-induced contraction of human resistance arteries." Clinical Science 81, s25 (1991): 525–29. http://dx.doi.org/10.1042/cs0810525.

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1. Using a Mulvany-Halpern myograph to measure changes in isometric tension, we have investigated the effect of ouabain on noradrenaline-induced contraction of human subcutaneous resistance arteries. 2. Low concentrations of ouabain (10 nmol/l or less) were shown not to alter vascular smooth muscle contractility or sensitivity to noradrenaline. 3. In contrast, higher concentrations of ouabain (100 nmol/l or more) were found to depress vascular smooth muscle contractility and to reduce the sensitivity of the noradrenaline concentration-response relationship. 4. These findings may have implicati

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Dahan, Diana, Mari Ekman, Anna-Karin Larsson-Callerfelt, et al. "Induction of angiotensin-converting enzyme after miR-143/145 deletion is critical for impaired smooth muscle contractility." American Journal of Physiology-Cell Physiology 307, no. 12 (2014): C1093—C1101. http://dx.doi.org/10.1152/ajpcell.00250.2014.

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MicroRNAs have emerged as regulators of smooth muscle cell phenotype with a role in smooth muscle-related disease. Studies have shown that miR-143 and miR-145 are the most highly expressed microRNAs in smooth muscle cells, controlling differentiation and function. The effect of miR-143/145 knockout has been established in the vasculature but not in smooth muscle from other organs. Using knockout mice we found that maximal contraction induced by either depolarization or phosphatase inhibition was reduced in vascular and airway smooth muscle but maintained in the urinary bladder. Furthermore, a

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Lazzam, Charles, Ron G. Carere, Christine Forster, et al. "Angioplasty produces marked and persistent impairment of vascular contractility." Journal of the American College of Cardiology 17, no. 2 (1991): A369. http://dx.doi.org/10.1016/0735-1097(91)92442-o.

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Sanbe, Atsushi, Yoshio Tanaka, Yoko Fujiwara, et al. "Enhanced vascular contractility in alpha1-adrenergic receptor-deficient mice." Life Sciences 84, no. 21-22 (2009): 713–18. http://dx.doi.org/10.1016/j.lfs.2009.02.020.

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Mulvany, M. J. "Vascular Structure and Smooth Muscle Contractility in Experimental Hypertension." Journal of Cardiovascular Pharmacology 10 (1987): S79—S85. http://dx.doi.org/10.1097/00005344-198700106-00010.

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Mulvany, M. J. "Vascular Structure and Smooth Muscle Contractility in Experimental Hypertension." Journal of Cardiovascular Pharmacology 10 (1987): S79—S85. http://dx.doi.org/10.1097/00005344-198706106-00010.

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