Relevant bibliographies by topics / Arteries Muscle contraction

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Arteries Muscle contraction'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 February 2022

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Journal articles on the topic "Arteries Muscle contraction"

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Jin, N., and R. A. Rhoades. "Activation of tyrosine kinases in H2O2-induced contraction in pulmonary artery." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 6 (1997): H2686—H2692. http://dx.doi.org/10.1152/ajpheart.1997.272.6.h2686.

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Hydrogen peroxide (H2O2) is an important reactive oxygen species implicated in lung vascular constriction and injury. The purpose of this study was to investigate the role of tyrosine kinases in H2O2-induced vascular contraction and dysfunction. In our study, H2O2 (200 microM) caused an initial transient contraction followed by a strong, sustained contraction in isolated rat pulmonary arteries. Genistein, a tyrosine kinase inhibitor, attenuated both the initial and the sustained contractions. Aminogenistein and tyrphostin 51, specific inhibitors of tyrosine kinases, had the same effects as gen
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Pelaez, Nancy J., Tracey R. Braun, Richard J. Paul, Richard A. Meiss, and C. Subah Packer. "H2O2 mediates Ca2+- and MLC20phosphorylation-independent contraction in intact and permeabilized vascular muscle." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 3 (2000): H1185—H1193. http://dx.doi.org/10.1152/ajpheart.2000.279.3.h1185.

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One purpose of the current study was to establish whether vasoconstriction occurs in all vessel types in response to H2O2. Isometric force was measured in pulmonary venous and arterial rings, and isobaric contractions were measured in mesenteric arteries and veins in response to H2O2. A second purpose was to determine whether H2O2-induced contraction is calcium independent. The addition of H2O2 to calcium-depleted (using the Ca2+ ionophore ionomycin in zero calcium EGTA buffer) muscle caused contraction. Furthermore, permeabilized muscle contracted in response to H2O2 even in zero Ca2+. The fi
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Xiao, Daliao, and Lubo Zhang. "ERK MAP kinases regulate smooth muscle contraction in ovine uterine artery: effect of pregnancy." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 1 (2002): H292—H300. http://dx.doi.org/10.1152/ajpheart.2002.282.1.h292.

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The present study investigated the potential role of extracellular signal-regulated kinase (ERK) in uterine artery contraction and tested the hypothesis that pregnancy upregulated ERK-mediated function in the uterine artery. Isometric tension in response to phenylephrine (PE), serotonin (5-HT), phorbol 12,13-dibutyrate (PDBu), and KCl was measured in the ring preparation of uterine arteries obtained from nonpregnant and near-term (140 days gestation) pregnant sheep. Inhibiting ERK activation with PD-98059 did not change the KCl-evoked contraction but significantly inhibited the contraction to
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Copp, Steven W., Joyce S. Kim, Victor Ruiz-Velasco, and Marc P. Kaufman. "The mechano-gated channel inhibitor GsMTx4 reduces the exercise pressor reflex in rats with ligated femoral arteries." American Journal of Physiology-Heart and Circulatory Physiology 310, no. 9 (2016): H1233—H1241. http://dx.doi.org/10.1152/ajpheart.00974.2015.

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Mechanical and metabolic stimuli arising from contracting muscles evoke the exercise pressor reflex. This reflex is greater in a rat model of simulated peripheral arterial disease in which a femoral artery is chronically ligated than it is in rats with freely perfused femoral arteries. The role played by the mechanically sensitive component of the exaggerated exercise pressor reflex in ligated rats is unknown. We tested the hypothesis that the mechano-gated channel inhibitor GsMTx4, a relatively selective inhibitor of mechano-gated Piezo channels, reduces the exercise pressor reflex in decereb
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Watanabe, Yoshimasa, Frank M. Faraci, and Donald D. Heistad. "Activation of Rho-associated kinase during augmented contraction of the basilar artery to serotonin after subarachnoid hemorrhage." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 6 (2005): H2653—H2658. http://dx.doi.org/10.1152/ajpheart.00923.2004.

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Delayed cerebral vasospasm after subarachnoid hemorrhage (SAH) may be due, in part, to altered regulation of arterial smooth muscle contraction. Contraction of cerebral arteries to serotonin is augmented after experimental SAH. We hypothesized that activation of Rho-associated kinase (Rho kinase) contributes to augmented contraction of cerebral arteries to serotonin after SAH. Autologous arterial blood (SAH) or artificial cerebrospinal fluid (control) was injected into the cisterna magna of anesthetized rabbits. At 2 days after injection, the basilar artery was excised and isometric contractio
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Fujii, Satoshi, and Kazuhiko Fujitsu. "Experimental vasospasm in cultured arterial smooth-muscle cells." Journal of Neurosurgery 69, no. 1 (1988): 92–97. http://dx.doi.org/10.3171/jns.1988.69.1.0092.

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✓ Smooth-muscle cells were cultured from rat aortic media, then oxyhemoglobin and other agents including serotonin, norepinephrine, and angiotensin II were added separately to the medium. Contractile and ultrastructural changes of the cells were examined with electron microscopy during the first 2 weeks of incubation. Oxyhemoglobin not only produced progressive contraction of the arterial smooth-muscle cells, but it also caused ultrastructural changes that resembled myonecrosis. In contrast, there was no evidence of progressive contraction or ultrastructural changes either in control cultures
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Löhn, Matthias, Dietmar Kämpf, Chai Gui-Xuan, Hermann Haller, Friedrich C. Luft, and Maik Gollasch. "Regulation of arterial tone by smooth muscle myosin type II." American Journal of Physiology-Cell Physiology 283, no. 5 (2002): C1383—C1389. http://dx.doi.org/10.1152/ajpcell.01369.2000.

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The initiation of contractile force in arterial smooth muscle (SM) is believed to be regulated by the intracellular Ca2+concentration and SM myosin type II phosphorylation. We tested the hypothesis that SM myosin type II operates as a molecular motor protein in electromechanical, but not in protein kinase C (PKC)-induced, contraction of small resistance-sized cerebral arteries. We utilized a SM type II myosin heavy chain (MHC) knockout mouse model and measured arterial wall Ca2+ concentration ([Ca2+]i) and the diameter of pressurized cerebral arteries (30–100 μm) by means of digital fluorescen
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Karibe, A., J. Watanabe, S. Horiguchi, et al. "Role of cytosolic Ca2+ and protein kinase C in developing myogenic contraction in isolated rat small arteries." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 3 (1997): H1165—H1172. http://dx.doi.org/10.1152/ajpheart.1997.272.3.h1165.

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Cytosolic Ca2+ and protein kinase C (PKC) may regulate the myogenic contraction of arterial myocytes. The role of these second messengers is examined in skeletal muscle small arteries, which have strong myogenic activity, and mesenteric small arteries, which have weak myogenic activity. The vessels were isolated and cannulated. The inner diameter was measured with a video-digitizing system. Cytosolic Ca2+ concentration was assessed by fura 2. Skeletal muscle small arteries dilated from 122 +/- 6 to 153 +/- 6 microm immediately after the transmural pressure change from 40 to 100 mmHg and constr
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Lash, J. M., and A. A. Shoukas. "Pressure dependence of baroreceptor-mediated vasoconstriction in rat skeletal muscle." Journal of Applied Physiology 70, no. 6 (1991): 2551–58. http://dx.doi.org/10.1152/jappl.1991.70.6.2551.

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To determine whether microvessels in resting or contracting skeletal muscle constrict during baroreceptor activation, vascular diameters were measured in the spinotrapezius muscle of adult rats (n = 12) during occlusion of the common carotid arteries. Neural and myogenic components were distinguished using two types of occlusion: 1) "normal" (arterial pressure was allowed to increase with baroreceptor activation) and 2) "isobaric" (arterial pressure was maintained constant by decreasing blood volume). During normal occlusions, intermediate and small arteriolar diameters decreased in resting an
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Virsolvy, Anne, Aurélie Fort, Lucie Erceau, et al. "Hypoxic Conditions Promote Rhythmic Contractile Oscillations Mediated by Voltage-Gated Sodium Channels Activation in Human Arteries." International Journal of Molecular Sciences 22, no. 5 (2021): 2570. http://dx.doi.org/10.3390/ijms22052570.

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Arterial smooth muscle exhibits rhythmic oscillatory contractions called vasomotion and believed to be a protective mechanism against tissue hypoperfusion or hypoxia. Oscillations of vascular tone depend on voltage and follow oscillations of the membrane potential. Voltage-gated sodium channels (Nav), responsible for the initiation and propagation of action potentials in excitable cells, have also been evidenced both in animal and human vascular smooth muscle cells (SMCs). For example, they contribute to arterial contraction in rats, but their physiopathological relevance has not been establis
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Dissertations / Theses on the topic "Arteries Muscle contraction"

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Wadsworth, R. M. "Regulation of contraction of arterial smooth muscle." Thesis, University of Strathclyde, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248764.

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Khabbaza, Elias Joseph. "Regulation of contraction in porcine coronary arteries /." The Ohio State University, 1987. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487325740717536.

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Betts, Luisa C. "Cellular events underlying endothelin-1-induced contraction of renal arteries." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342244.

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Aaker, Aaron Paul. "Vasomotor responses of rat skeletal muscle arterioles to norepinephrine and adenosine." free to MU campus, to others for purchase, 2001. http://wwwlib.umi.com/cr/mo/fullcit?p3012943.

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Browne, Brendan. "Role of ROCK and PKC in regulation of contraction of permeabilized femoral arterial smooth muscle." VCU Scholars Compass, 2009. http://scholarscompass.vcu.edu/etd/1668.

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KCl is traditionally used as a stimulus to examine the role of increases in cytosolic Ca2+ on the regulation of smooth muscle contraction. KCl bypasses GPCR activation, thereby avoiding activation of additional cell signaling systems, such as phospholipase C and PKC that are inherent to Gaq and Ga12/13 stimulation. GPCR activation causes Ca2+ sensitization (greater force for a given increase in Ca2+) by a ROCK- and PKC-dependent inhibition of myosin light chain (MLC) phosphatase. Recent studies have demonstrated that KCl can also produce Ca2+ sensitization, implying that Ca2+ itself may induce
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Zhao, Weimin. "Controle de la contraction musculaire lisse, bronchique et vasculaire pulmonaire : roles du métabolisme energétique et du monoxyde d'azote." Bordeaux 2, 1995. http://www.theses.fr/1995BOR28326.

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Greyner, Henry José. "The role of prostaglandins, nitric oxide and oxygen in the ductus arteriosi of the pre-term chicken embryo (Gallus domesticus)." Thesis, University of North Texas, 2007. https://digital.library.unt.edu/ark:/67531/metadc5173/.

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The chicken ductus arteriosi (DA) are two embryonic blood vessels that shunt blood away from the non-ventilated lungs and towards the body and chorioallantoic membrane. I show that prostaglandins have a diminished role in maintaining chicken DA patency and nitric oxide inhibits oxygen induced contraction of the day 19 proximal DA in a time dependent manner. The pathways governing oxygen induced contraction in the chicken DA are similar to those found in mammals and include contributions from ROS, Kv channels, L-type Ca2+ channels, and the Rho kinase pathway. Longer exposure to high oxygen gen
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Saïag, Bernard. "Modulation de l'etat contractile du muscle lisse vasculaire par les purines, les pyrimidines et leurs recepteurs." Rennes 1, 1989. http://www.theses.fr/1989REN1A052.

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Etude de la modulation de l'etat contractile des muscles lisses arteriels (arteres caudale et femorale du rat) et veineux (veines saphene et maxillaire interne du chien) par des molecules de nature purique (adenosine. . . Atp) ou pyrimidique (utp)
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Armstrong, Michelle Hine, Tepole Adrián Buganza, Ellen Kuhl, Bruce R. Simon, and Geest Jonathan P. Vande. "A Finite Element Model for Mixed Porohyperelasticity with Transport, Swelling, and Growth." Public Library of Science, 2016. http://hdl.handle.net/10150/614631.

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The purpose of this manuscript is to establish a unified theory of porohyperelasticity with transport and growth and to demonstrate the capability of this theory using a finite element model developed in MATLAB. We combine the theories of volumetric growth and mixed porohyperelasticity with transport and swelling (MPHETS) to derive a new method that models growth of biological soft tissues. The conservation equations and constitutive equations are developed for both solid-only growth and solid/fluid growth. An axisymmetric finite element framework is introduced for the new theory of growing MP
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Gonzalez, de la Fuente Patrick. "Physiopathologie cellulaire du muscle lisse vasculaire pulmonaire : rôle de l'influx calcique capacitif et effet de l'hypoxie." Bordeaux 2, 1995. http://www.theses.fr/1995BOR28373.

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Books on the topic "Arteries Muscle contraction"

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Bochaton-Piallat, Marie-Luce, Carlie J. M. de Vries, and Guillaume J. van Eys. Vascular smooth muscle cells. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0007.

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To understand the function of arteries in the regulation of blood supply throughout the body it is essential to realize that the vessel wall is composed predominantly of smooth muscle cells (SMCs) with only one single layer of luminal endothelial cells. SMCs determine the structure of arteries and are decisive in the regulation of blood flow. This review describes the reason for the large variation of SMCs throughout the vascular tree. This depends on embryonic origin and local conditions. SMCs have the unique capacity to react to these conditions by modulating their phenotype. So, in one situ
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Book chapters on the topic "Arteries Muscle contraction"

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Ohanian, J., F. Statham, L. Shaw, S. White, A. M. Heagerty, and V. Ohanian. "Protein Kinase C and Contraction of Vascular Smooth Muscle." In The Resistance Arteries. Humana Press, 1994. http://dx.doi.org/10.1007/978-1-4757-2296-3_6.

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Nakayama, Koichi, and Yoshio Tanaka. "Myogenic Contraction and Relaxation of Arterial Smooth Muscle." In Essential Hypertension 2. Springer Japan, 1989. http://dx.doi.org/10.1007/978-4-431-68090-1_7.

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Rembold, Christopher M. "[Ca2+]i and Contraction of Arterial Smooth Muscle." In Ion Channels and Ion Pumps. Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4612-2596-6_8.

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Rembold, Christopher M., and Richard A. Murphy. "Arterial Smooth Muscle Contraction Is Dependent on Sustained Increases in Myoplasmic Ca2+." In Essential Hypertension 2. Springer Japan, 1989. http://dx.doi.org/10.1007/978-4-431-68090-1_5.

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Bruschi, G., M. E. Bruschi, G. Regolisti, and A. Borghetti. "Changes in Ca2+ and Ca2+ Sensitivity During Contraction-Relaxation of Arterial Muscle." In Cellular Aspects of Hypertension. Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-662-00983-3_7.

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Itoh, Takeo, Yoshimasa Watanabe, Makoto Yoshida, and Akito Suzuki. "Role of Protein Kinase C in the G Protein-Mediated Increase in Myofilament Ca2+ Sensitivity in Skinned Arterial Smooth Muscle of the Rabbit." In Regulation of the Contractile Cycle in Smooth Muscle. Springer Japan, 1995. http://dx.doi.org/10.1007/978-4-431-65880-1_5.

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Heinle, H. "Influence of Oxidative Stress on Metabolic and Contractile Functions of Arterial Smooth Muscle." In Oxygen Sensing in Tissues. Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-83444-8_13.

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Bruining, Nico, Eric Boersma, and Dirk J. Duncker. "Regulation of coronary flow." In State of the Art Surgical Coronary Revascularization, edited by David P. Taggart, John D. Puskas, and Mario Gaudino. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198758785.003.0003.

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This chapter describes the regulation of coronary blood flow. The left ventricle generates the systemic arterial blood pressure that is required to maintain coronary blood flow. The coronary circulation is unique among regional vascular beds in that its perfusion is impeded during the systolic phase of the cardiac cycle by the surrounding contracting cardiac muscle. Systolic contraction increases left ventricular wall tension and compresses the intramyocardial microvessels, thereby impeding coronary arterial inflow. This compression is not uniformly distributed across the left ventricular wall, resulting in a redistribution of blood flow from the subendocardium to subepicardium.
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Mitchell, Graham. "The Blood Pressure of Giraffes." In How Giraffes Work. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780197571194.003.0009.

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As discussed in this chapter, giraffes have, compared with any other mammal, a very high mean blood pressure of ~250 mmHg. Human blood pressure is ~90 mmHg. Its size is determined by the length of the neck, the height of the head above the heart, by hydrostatic pressure generated by gravity acting on the column of blood in the carotid artery, and contractions of the heart muscles: blood pressure must be high enough to ensure that blood reaches the brain. Uniquely in giraffes blood pressure is regulated by receptors that are located in both the carotid and occipital arteries. Once thought to be ~2.5% of body mass the heart is smaller (~0.5% of body mass) but its muscle walls, especially of the interventricular wall and left ventricle wall, are exceptionally thick (up to 8 cm). The relative cardiac output is the same as in other mammals (~5 L 100 kg<sup>–1</sup> of body mass) through a combination of a higher than predicted heart rate (70 b min<sup>–1</sup> vs 50 b min<sup>–1</sup>) and smaller than predicted stroke volume (~0.7 ml kg<sup>–1</sup> body mass vs 1.2 ml kg<sup>–1</sup>). Stroke volume is small because the left ventricle muscle wall is thick. The origin of high blood pressure is the resistance to blood flow, which is about twice what it is in other mammals. The higher resistance results from a combination of the thick muscular walls and narrow lumens of a giraffe’s blood vessels and unique mechanisms that regulate blood flow to the brain.
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Conference papers on the topic "Arteries Muscle contraction"

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Janssens, W. J., and J. M. Van Nueten. "VASOCONSTRICTOR EFFECTS OF AGGREGATING PLATELETS IN RABBIT PULMONARY ARTERIES WITH AND WITHOUT ENDOTHELIUM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643354.

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The aim of the present experiments was to investigate the modulatory role of the endothelium on vasoconstrictions induced by aggregating platelets. Rings of rabbit pulmonary arteries were mounted for isometric tension recording. The presence or absence of the endothelium was confirmed using acetylcholine-induced relaxations. All contractions were expressed as percentage of a K+-induced (100 mM) contraction. Thrombin was administered to the preparations at 0.5 NIH units/ml. At this concentration the enzyme caused no or only very small contractions, but apparently induced maximal platelet activa
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Li, Yali, and N. C. Goulbourne. "Electro-Chemo-Mechanical Modeling of the Artery Myogenic Transient and Steady-State Response." In ASME 2014 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/imece2014-39237.

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Active contraction of smooth muscle results in the myogenic response and vasomotion of arteries, which adjusts the blood flow and nutrient supply of the organism. It is a multiphysic process coupled electrical and chemical kinetics with mechanical behavior of the smooth muscle. This paper presents a new constitutive model for the media layer of the artery wall to describe the myogenic response of artery wall for different transmural pressures. The model includes two major components: electrobiochemical, and chemomechanical parts. The electrochemical model is a lumped Hodgkin-Huxley-type cell m
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Scott, Devon, Robin Shandas, and Wei Tan. "Effect of Vessel Stiffening and High Pulsatility Flow on Contractile Function and Proliferation of Small Arterial Cells." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19597.

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Recent studies have identified arterial stiffening as a predictor of some vascular diseases such as pulmonary hypertension, which is characterized by dysfunction of small arteries. Stiffening is shown to cause changes in blood flow, extending high pulsatile flow into small arteries that normally experience steady flow conditions (Chui 2004). However, few studies have investigated the mechanisms underlying the effects of arterial stiffening on vascular remodeling. We hypothesized that arterial stiffness effects dysfunction of downstream vascular endothelium and smooth muscle through changes in
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Agianniotis, Aristotelis, Alexander Rachev, and Nikos Stergiopulos. "Active Axial Stress in Mouse Aorta." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80102.

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Arteries exhibit a complex mechanical behavior due to their complex structure and composition. When smooth muscle cells (SMCs) are stimulated to contract, an artery constricts and develops the so called active stress in the arterial wall. Assuming that the SMCs are oriented in the circumferential direction most of studies consider solely development of the circumferential active stress [1]. However, histological findings show existence of SMCs oriented in both the circumferential and axial direction; these vessels manifest biaxial contractile response [2, 3]. In this study we also observed bia
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Agianniotis, Aristotelis, Alexander Rachev, and Nikos Stergiopulos. "A Biomechanical Model for the Biaxial Effect of the Contraction of Muscle Cells." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53091.

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The arterial tissue consists of elastin and collagen which develop passive stresses in the arterial wall, and muscle cells that develop active stresses when are appropriately stimulated. Earlier model for the active properties of the arterial wall, where the muscle cells orientation is assumed circumferential, failed in describing accurately the tissue response to inflation-extension loading. It has been hypothesized that the development of active stresses in both circumferential and longitudinal directions could overcome this shortcoming. Inflation-extension tests on common carotids of rabbit
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Du, Wei, Kenneth M. Pryse, Judy A. Fee, Elliot L. Elson, and Ruth J. Okamoto. "Vascular Smooth Muscle Cell Mechanics During Cyclic Stretch: Effect of Serum and a Serum Substitute." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176205.

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Remodeling of arteries in response to altered loads is an area of intense interest to cardio-vascular clinicians and researchers. In humans, changes due to cardiovascular diseases (e.g. aortic dilatation) may occur slowly over many years, and mathematical models that describe the remodeling response are needed for predicting the course, and possible treatment, of these diseases. Recently, Humphrey and co-workers have proposed constrained mixture models [1] that consider local stresses in the arterial wall to be the sum of contributions from collagen, elastic fibers, and vascular smooth muscle
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Demolle, D., E. J. Cragoe, and J. M. Boeynaems. "MECHANISMS INVOLVED IN 5-HT STIMULATION OF PROSTACYCLIN PRODUCTION BY BOVINE AORTIC SMOOTH MUSCLE CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642841.

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Serotonin (5-HT) stimulates prostacyclin (PGI2) production by bovine aortic smooth muscle cells in culture via 5-HT2 receptors (1). These cells express a synthetic phenotype (2), whereas the majority of the smooth muscle cells in the media from adult arteries are in a contractile state. We have now shown that 5-HT (1-10 μM) also stimulates PGI2 production by a preparation of contractile smooth muscle cells : explants from bovine aortic media cultured for short periods. This effect is independent from 5-HT2 receptors : it is only partially inhibited (±30%) by ketan-serin (a selective and potent
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Vanhoutte, Paul M. "PLATELETS, ENDOTHELIUM AND VASOSPASM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643722.

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The endothelium can secrete both relaxing and contracting substances. One of the most powerful stimuli to the release of the former are thrombin and aggregating platelets. This contributes to the protective role of the endothelium against inappropriate intraluminal platelet aggregation and coagulation in blood vessels with an intact intima. Thrombin-induced, endothelium-dependent relaxations have been obtained in isolated arteries of different species, including humans. Endothelium-dependent relaxations can be evoked by autologous platelets in isolated blood vessels of the dog, pig and rat; th
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Zhou, Boran, Alexander Rachev, and Tarek Shazly. "Active Stress in the Porcine Renal Artery." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14427.

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As a typical muscular conduit artery, the renal artery manifests an active response when the vascular smooth muscle is stimulated to contract. To present there are few experimental data [1] and no constitutive formulation of the renal arterial tissue that accounts for the active stress developed when the smooth muscle cells (SMCs) are stimulated to contract. Most studies identify the circumferential and axial active stresses by processing the in-vitro experimentally recorded change in diameter and axial force in a tubular arterial specimen inflated by an internal pressure, kept at constant axi
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Chen, J., M. Rodriguez, N. Lai, et al. "Mechanosensitive Channel Piezo1 in the Transition of Pulmonary Arterial Smooth Muscle Cells from a Contractile to a Proliferative Phenotype." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a3669.

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