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Tuesday, April 14, 2020 | History

2 edition of Mechanisms of agonsit-induced calcium sensitisation in small arteries. found in the catalog.

Mechanisms of agonsit-induced calcium sensitisation in small arteries.

Linda Mary Shaw

Mechanisms of agonsit-induced calcium sensitisation in small arteries.

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Published by University of Manchester in Manchester .
Written in English


Edition Notes

Thesis (Ph.D.), University of Manchester, Faculty of Medicine.

ContributionsUniversity of Manchester. Faculty of Medicine.
The Physical Object
Pagination223p.
Number of Pages223
ID Numbers
Open LibraryOL16435676M

Arterial smooth muscle constriction in response to pressure, i.e., myogenic tone, may involve calcium-dependent and calcium-sensitization mechanisms. Calcium sensitization in vascular smooth muscle is regulated by kinases such as PKC and Rho kinase, and activity of these kinases is known to be altered in cardiovascular by: MLCP activity is modulated through two agonist-induced mechanisms in a process called calcium sensitization. First, it is controlled by the inhibitory action of diacylglycerol (DAG), another second messenger, which also results from the hydrolyzation of PIP by: Vasodilation is the widening of blood vessels. It results from relaxation of smooth muscle cells within the vessel walls, in particular in the large veins, large arteries, and smaller process is the opposite of vasoconstriction, which is the narrowing of blood vessels.. When blood vessels dilate, the flow of blood is increased due to a decrease in vascular resistance and.   Effects on calcium induced contraction and calcium sensitization The effects of DG on the calcium channel were investigated in a calcium-free, high-[+] depolarizing Kreb's solution. The subsequent increase in the concentration of [2] ( .


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Mechanisms of agonsit-induced calcium sensitisation in small arteries. by Linda Mary Shaw Download PDF EPUB FB2

We conclude that it is unlikely that a ubiquitous abnormality of the sensitivity of the contractile apparatus to Ca 2+ or agonist-induced Ca 2+ sensitization in vascular smooth muscle underlies the elevated total peripheral resistance associated with by:   Activation of Ca 2+ Sensitization Mechanisms in Gastrointestinal Smooth Muscles.

Much of the evidence for Ca 2+ sensitization in GI smooth muscles comes from studies examining the effects of ROCK or PKC inhibitors, or other kinase inhibitors, on agonist-evoked contractile by:   Mechanisms of Ca 2+ sensitization of force production by noradrenaline were investigated by measuring contractile responses, intracellular Ca 2+ concentration ([Ca 2+ ] i) and phosphorylation of the myosin light chain (MLC) in intact and α-toxin-permeabilized rat mesenteric small by: In left anterior descending coronary arteries taken from adult male Wistar rats, T abolishes +/% of calcium-dependent contraction induced by potassium chloride, +/% of the mostly.

We determined the calcium signalling pathways involved in the mechanisms of contraction of the vasoconstrictive agonists KCl, U and PDBu in isolated human mesenteric arteries. The influence of gender, vessel diameter and age of the patients was also by:   AbstractThe contraction of detrusor smooth muscles depends on the increase in intracellular calcium.

The influx of calcium from the plasma membrane calcium channels and calcium release from the sarcoplasmic reticulum give rise to intracellular calcium. Under the pathophysiological conditions, the increased sensitivity of regulatory and contractile proteins to calcium also plays an Cited by: 3.

Changes of calcium mobilization and calcium-sensitization mechanism in vascular smooth muscle cells in hypertension Article in Chinese Pharmacological Bulletin 30(2) February with. Mechanisms of agonist-induced constriction in isolated human mesenteric arteries Article in Vascular Pharmacology 44(6) June with 12 Reads How we measure 'reads'.

Thus, the present study investigated the vessel reactivity of FA in different vascular beds including aortic arteries, small mesenteric arteries and coronary arteries. And whether its underlying mechanisms were related to calcium channel and calcium sensitization signaling pathway were also studied both in various arteries, vascular endothelial cells and smooth muscle by: 6.

Concentration-response curves of histamine-induced contraction in arterial tissue-engineered vascular media (TEVM) rings in the presence of (A) the myosin light chain kinase inhibitor, ML-9 (10 μM), (B) the Rho-kinase inhibitor, Y ( μM), and (C) the protein kinase C Cited by:   The small GTPase Rho and its target, Rho-associated kinase, participate in this latter mechanism in vitro4,5,6, but their participation has not been demonstrated in intact muscles.

Here we show that a pyridine derivative, Y, selectively inhibits smooth-muscle contraction by inhibiting Ca 2+ by: It was hypothesized that NaF induces calcium sensitization in Ca 2+ -controlled solution in permeabilized rat mesenteric arteries. Rat mesenteric arteries were permeabilized with β-escin and subjected Mechanisms of agonsit-induced calcium sensitisation in small arteries.

book tension by: 8. attenuation of a greater calcium sensitization at normal calcium entry but also due to the attenuation of a normal calcium sensitization at a greater calcium entry. The above mentioned facts might considerably complicate the evaluation of the role of these two pathways in BP control.

Fig. The schematic representation of the principal pathways. Ferulic acid, a Mechanisms of agonsit-induced calcium sensitisation in small arteries. book ingredient presents in several Chinese Materia Medica such as Radix Angelicae Sinensis, has been identified as an important mu Cited by: 6.

NaF induces calcium sensitization in a Ca(2+)-dependent manner in beta-escin-permeabilized rat mesenteric arteries. These results suggest that NaF is an activator of the Rho kinase signaling.

Introduction. Calcium signaling in smooth muscle is a varied affair. The types of local and global calcium signals, the release process from the internal calcium store (SR, Sarcoplasmic Reticulum), and the calcium homeostatic control mechanisms found in this one cell type encompass most of the mechanisms only found separately in other cell by: 1.

Our understanding of the cellular signalling mechanisms contributing to agonist‐induced constriction is almost exclusively based on the study of conduit arteries. Resistance arteries/arterioles have received less attention as standard biochemical approaches lack the necessary sensitivity to permit quantification of phosphoprotein levels in Cited by: vasoconstriction in penile small arteries involves Ca2 entry through both L-type and 2-APB-sensitive receptor-operated channels, as well as Ca2 sensitization mechanisms mediated by PKC, TK, and RhoK.

A capacitative Ca2 entry coupled to noncontractile functions of the smooth muscle cell is. Ca2+ sensitization by the Rho/Rho-kinase pathway contributes to the tonic phase of agonist-induced contraction in smooth muscle, and abnormally increased activation of myosin II by this mechanism.

Thiazide-Like Diuretics Attenuate Agonist-Induced Vasoconstriction by Calcium Desensitization Linked to Rho Kinase Zhiming Zhu, Shanjun Zhu, Daoyan Liu, Tingbing Cao, Lijuan Wang, Martin Tepel Abstract—Lowering blood pressure using thiazide-like diuretics, including chlorthalidone and hydrochlorothiazide, has.

The observed calcium sensitization appears to result from an increase in myosin light chain phosphorylation and is mediated by a mechanism(s) independent of the tyrosine kinase pathway which has been proposed to mediate the ET-1 induced increase in myofilament Ca 2+ sensitivity in systemic arteries (Ohanian et al., ).Cited by:   An hypothesis for the mechanisms of adrenergic activation of small arteries is advanced.

This involves asynchronous Ca 2+ waves in individual SMC, synchronous Ca 2+ oscillations (at high levels of adrenergic activation), Ca 2+ sparks, “Ca 2+ -sensitization” by PKC and Rho-associated kinase (ROK), and thin filament by: Thiazide-like diuretics have been the cornerstone in hypertension management for several years.

Recent data from the Antihypertensive and Lipid-Lowering to prevent Heart Attack Trial (ALLHAT) showed that blood pressure lowering using thiazide-like diuretics had beneficial effects, including fewer events for all cardiovascular diseases, stroke, and heart failure compared with an angiotensin Cited by: The major mechanism for vascular smooth muscle calcium elevation during stretch is presumed to involve release from intracellular stores in (6, 18, 20) and/or inflow through voltage-dependent calcium channels on activation of cation channels (21, 34).

In the present study, however, the amplitude and baseline of the lymphatic smooth muscle Cited by: Human isolated subcutaneous arteries were mounted in a myograph and isometric tension measured. In some experiments, intracellular calcium [Ca 2+] i was also measured using fura‐ Angiotensin II ( p M – 1 μ M) increased [Ca 2+] i and tone in a concentration‐dependent manner.

The effects of angiotensin II ( n M) were inhibited by an AT 1 ‐receptor antagonist, candesartan ( p M).Cited by: At birth, associated with the rise in oxygen levels, the resistance pulmonary arteries (PA) dilate and the ductus arteriosus (DA) constricts.

In neonatal and adult life, hypoxia in the small airways causes pulmonary vasoconstriction (HPV) which helps to direct mixed venous blood Cited by:   Our understanding of the cellular signalling mechanisms contributing to agonist-induced constriction is almost exclusively based on the study of conduit arteries.

Resistance arteries/arterioles have received less attention as standard biochemical approaches lack the necessary sensitivity to permit quantification of phosphoprotein levels in these small by: Abstract—Pressure-induced activation of vascular smooth muscle may involve electromechanical as well as nonelectromechanical coupling compared calcium-tone relations of cannulated rat mesenteric small arteries during pressure-induced activation, depolarization (16 to 46 mmol/L K +), and α 1-adrenergic stimulation (1 μmol/L phenylephrine).Cited by:   In pressurised rat mesenteric small arteries (50 mmHg), we examined the effects of stimulation with U, endothelin‐1 (ET‐1) or phenylephrine (PE) on changes in vessel diameter, global [Ca 2+] i, individual smooth muscle cell [Ca 2+] i and Ca 2+ ‐sensitisation of contraction.

U or ET‐1 gave tonic diameter reductions, whereas PE‐stimulated vessels gave tonic contractions or Cited by: Regulation of cytosolic calcium and myofilament calcium sensitivity varies considerably with postnatal age in cerebral arteries.

Because these mechanisms also govern myogenic tone, the present study used graded stretch to examine the hypothesis that myogenic tone is less dependent on calcium influx and more dependent on myofilament calcium sensitization in term fetal compared with adult. The present study was aimed to characterize the effects of ageing on vascular contraction by noradrenaline in rat isolated arteries.

The existence of vascular bed heterogeneity was investigated in endothelium‐denuded conductance (aorta) and resistance (small mesenteric artery, SMA) arteries, with respect to Ca 2+ handling, Ca 2+ sensitization or Ca 2+ ‐independent by: The second mechanism of MLCP inhibition is through phosphorylation of smooth muscle-specific MLCP inhibitor protein CPI 9 Although there are multiple sites to be phosphorylated, the phosphorylation at only Thr38 increases the inhibitory effect of CPI on MLCP by fold.

10 A major kinase for agonist-induced CPI phosphorylation at Cited by: The relationships between smooth muscle calcium and isometric tension generation to spontaneous lymphatic pump activity and its modulation by stretch equivalent from 0 to ∼6 cmH 2 O were investigated.

Excised preparations of the rat thoracic duct were mounted on a wire myograph and loaded with the calcium-sensitive fluorochrome indoCited by: The Objective of these studies is to define the mechanisms that regulate tone in equine small laminar arteries.

The major determinants of tone in vascular smooth muscle are the concentration of intracellular calcium and the sensitivity of the contractile apparatus to calcium. All these results suggest that arsenite increases agonist-induced vasoconstriction mediated by MLC phosphorylation in smooth muscles and that calcium sensitization is one of the key mechanisms for the hypercontraction induced by arsenite in blood vessels.

Microtubules constitute one of the main cytoskeletal components in eukaryotic cells. Recent studies have shown that microtubule disruption induced significant vasoconstriction or enhanced agonist-induced contraction in vascular smooth muscle.

However, the underlying mechanisms are not clear. We hypothesize that microtubule disruption may affect contractile signaling in vascular smooth Cited by: Inhibition of the Na,K-ATPase by ouabain potentiates vascular tone and agonist-induced contraction. These effects of ouabain varies between different reports.

In this study, we assessed whether the pro-contractile effect of ouabain changes with arterial diameter and the molecular mechanism behind it. Rat mesenteric small arteries of different diameters (– µm) were studied for Cited by: 2.

Myogenic tone of small arteries is dependent on the presence of extracellular calcium (), and, recently, a receptor that senses changes in Ca 2+, the calcium-sensing receptor (CaR), has been detected in vascular investigated whether the CaR is involved in the regulation of myogenic tone in rat subcutaneous small by: 1 Mechanisms of Ca2+ sensitization of force production by noradrenaline were investigated by measuring contractile responses, intracellular Ca2+ concentration ((Ca2+)i) and phosphorylation of the myosin light chain (MLC) in intact and α‐toxin‐permeabilized rat mesenteric small arteries.

2 The effects of noradrenaline were investigated at constant membrane potential by comparing fully. Mechanisms involved in Ca 2+ sensitization of contractile elements induced by the activation of muscarinic receptors in membrane‐permeabilized preparations of the rat proximal and distal colon were studied.

In α‐toxin‐permeabilized preparations from the rat proximal and distal colon, Ca 2+ induced a rapid phasic and subsequent tonic component. After Ca 2+ ‐induced contraction Cited by:.

19 Guibert C, Marthan R, and Savineau JP. 5-HT induces an arachidonic acid-sensitive calcium influx in rat small intrapulmonary artery. Am J Physiol Lung Cell Mol Physiol L–L, Link ISI Google Scholar; 20 Halaszovich CR, Zitt C, Jungling E, and Luckhoff A.

Inhibition of TRP3 channels by lanthanides. Block from the cytosolic Cited by: Buus CL, Aalkjær C, Nilsson H, et al.: Mechanisms of Ca2+ sensitization of force production by noradrenaline in rat mesenteric small arteries.

J PhysiolCited by: Calcium ions (Ca 2+) are present in low concentrations in the cytosol (~ nM) and in high concentrations (in mM range) in both the extracellular medium and intracellular stores (mainly sarco/endo/plasmic reticulum, SR).This differential allows the calcium ion to be a ubiquitous 2 nd messenger that carries information essential for cellular functions as diverse as contraction, Cited by: 7.