scholarly journals Influence of Constriction, Wall Tension, Smooth Muscle Activation and Cellular Deformation on Rat Resistance Artery Vasodilator Reactivity

2012 ◽  
Vol 29 (5-6) ◽  
pp. 883-892 ◽  
Author(s):  
Ilsley Colton ◽  
Maurizio Mandalà ◽  
Jude Morton ◽  
Sandra T. Davidge ◽  
George Osol
Keyword(s):  
Smooth Muscle ◽  
Muscle Activation ◽  
Wall Tension ◽  
Resistance Artery ◽  
Cellular Deformation

Unstable radii in muscular blood vessels

1996 ◽  
Vol 271 (6) ◽  
pp. H2669-H2676 ◽  
Author(s):  
C. M. Quick ◽  
H. L. Baldick ◽  
N. Safabakhsh ◽  
T. J. Lenihan ◽  
J. K. Li ◽  
...  
Keyword(s):  
Experimental Data ◽  
Smooth Muscle ◽  
Muscle Activation ◽  
Critical Level ◽  
Active Tension ◽  
Wall Tension ◽  
Equilibrium Pressure ◽  
Variable Level ◽  
Parabolic Function ◽  
Maximal Pressure

A model of a muscular blood vessel in equilibrium that predicts stable and unstable control of radius is presented. The equilibrium wall tension is modeled as the sum of a passive exponential function of radius and an active parabolic function of radius. The magnitude of the active tension is varied to simulate the variable level of smooth muscle activation. This tension-radius relationship is then converted to an equilibrium pressure-radius relationship via Laplace's law. This model predicts the traditional ability to control the radius below a critical level of activation. However, when the active tension is raised above this critical level, the pressure-radius relationship (with pressure plotted on the ordinate and radius on the abscissa) becomes N shaped with a relative maximal pressure (Pmax) and a relative minimal pressure (Pmin). For this N-shaped curve, there are three equilibrium radii for any pressure between Pmin and Pmax. Analysis shows that the middle radius is unstable and thus cannot be maintained at equilibrium. Previously unexplained experimental data reveal evidence of this instability.

Role of Cl− currents in rat aortic smooth muscle activation by prostaglandin F2α

2003 ◽  
Vol 481 (2-3) ◽  
pp. 133-140 ◽  
Author(s):  
Jihua Jiang ◽  
Peter H Backx ◽  
Hwee Teoh ◽  
Michael E Ward
Keyword(s):  
Smooth Muscle ◽  
Muscle Activation ◽  
Prostaglandin F2α ◽  
Aortic Smooth Muscle

scholarly journals Effect of pharmacologically induced smooth muscle activation on permeability in murine colitis

2003 ◽  
Vol 12 (1) ◽  
pp. 21-27 ◽  
Author(s):  
Freek J. Zijlstra ◽  
Marieke E. van Meeteren ◽  
Ingrid M. Garrelds ◽  
Maarten A.C. Meijssen
Keyword(s):  
Smooth Muscle ◽  
Intestinal Permeability ◽  
Muscle Activation ◽  
Tap Water ◽  
Water Solution ◽  
Smooth Muscles ◽  
Distal Colon ◽  
Mucosal Inflammation ◽  
Smooth Muscle Relaxation ◽  
Organ Bath

Background:Both intestinal permeability and contractility are altered in inflammatory bowel disease. Little is known about their mutual relation. Therefore, anin vitroorgan bath technique was developed to investigate the simultaneous effects of inflammation on permeability and smooth muscle contractility in different segments of the colon.Methods and materials:BALB/c mice were exposed to a 10% dextran sulphate sodium drinking water solution for 7 days to induce a mild colitis, while control mice received normal tap water. Intestinal segments were placed in an oxygenated organ bath containing Krebs buffer. Permeability was measured by the transport of the marker molecules3H-mannitol and14C-polyethyleneglycol 4000. Contractility was measured through a pressure sensor. Smooth muscle relaxation was obtained by salbutamol and l-phenylephrine, whereas contraction was achieved by carbachol and 1-(3-chlorophenyl)-biguanide.Results:The intensity of mucosal inflammation increased throughout the colon. Also, regional differences were observed in intestinal permeability. In both normal and inflamed distal colon segments, permeability was diminished compared with proximal colon segments and the non-inflamed ileum. Permeability in inflamed distal colon segments was significantly decreased compared with normal distal segments. Pharmacologically induced relaxation of smooth muscles did not affect this diminished permeability, although an increased motility positively affected permeability in inflamed and non-inflamed distal colon.Conclusions:Inflammation and permeability is inversely related. The use of pro-kinetics could counteract this disturbed permeability and, in turn, could regulate the disturbed production of inflammatory mediators.

Interleukin-1 beta alters actin expression and inhibits contraction of rat thoracic aorta

1992 ◽  
Vol 262 (4) ◽  
pp. C828-C833 ◽  
Author(s):  
L. A. Trinkle ◽  
D. Beasley ◽  
R. S. Moreland
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Protein Content ◽  
Muscle Activation ◽  
Smooth Muscle Actin ◽  
Interleukin 1 ◽  
Contractile Protein ◽  
Interleukin 1 Beta ◽  
Alpha Smooth Muscle Actin ◽  
Mlc Phosphorylation

Previous studies have indicated that interleukin-1 beta (IL-1) inhibits contraction of rat aortas by activating nitric oxide production in vascular smooth muscle cells, with subsequent increases in guanosine 3',5'-cyclic monophosphate (cGMP). This study determined if the effect of IL-1 involves the primary regulatory event in smooth muscle activation, myosin light chain (MLC) phosphorylation. This study also examined whether IL-1 affects contractile protein content. IL-1 (20 ng/ml) significantly decreased stress in response to 0.1 microM phenylephrine with a concomitant decrease in MLC phosphorylation. Incubation with IL-1 for 3 h or longer decreased alpha-smooth muscle actin and increased gamma-actin isoform, with no change in beta-nonmuscle actin or myosin isozyme content. These results suggest that IL-1 inhibition of a vascular smooth muscle contraction may be due to a decrease in activator calcium, which may account for the resultant decrease in MLC phosphorylation. These results also indicate that IL-1 significantly affects contractile protein content, enhancing gamma-actin isoforms and decreasing the vascular smooth muscle specific alpha-isoactin.

scholarly journals Role of smooth muscle activation in the static and dynamic mechanical characterization of human aortas

2022 ◽  
Vol 119 (3) ◽  
pp. e2117232119
Author(s):  
Giulio Franchini ◽  
Ivan D. Breslavsky ◽  
Francesco Giovanniello ◽  
Ali Kassab ◽  
Gerhard A. Holzapfel ◽  
...  
Keyword(s):  
Experimental Data ◽  
Smooth Muscle ◽  
Muscle Activation ◽  
Mechanical Response ◽  
Mechanical Characterization ◽  
Viscoelastic Behavior ◽  
Material Model ◽  
Suitable Material ◽  
Dynamic Mechanical

Experimental data and a suitable material model for human aortas with smooth muscle activation are not available in the literature despite the need for developing advanced grafts; the present study closes this gap. Mechanical characterization of human descending thoracic aortas was performed with and without vascular smooth muscle (VSM) activation. Specimens were taken from 13 heart-beating donors. The aortic segments were cooled in Belzer UW solution during transport and tested within a few hours after explantation. VSM activation was achieved through the use of potassium depolarization and noradrenaline as vasoactive agents. In addition to isometric activation experiments, the quasistatic passive and active stress–strain curves were obtained for circumferential and longitudinal strips of the aortic material. This characterization made it possible to create an original mechanical model of the active aortic material that accurately fits the experimental data. The dynamic mechanical characterization was executed using cyclic strain at different frequencies of physiological interest. An initial prestretch, which corresponded to the physiological conditions, was applied before cyclic loading. Dynamic tests made it possible to identify the differences in the viscoelastic behavior of the passive and active tissue. This work illustrates the importance of VSM activation for the static and dynamic mechanical response of human aortas. Most importantly, this study provides material data and a material model for the development of a future generation of active aortic grafts that mimic natural behavior and help regulate blood pressure.

Impedance, gas mixing, and bimodal ventilation in constricted lungs

2003 ◽  
Vol 94 (3) ◽  
pp. 1003-1011 ◽  
Author(s):  
Ron C. Anafi ◽  
Kenneth C. Beck ◽  
Theodore A. Wilson
Keyword(s):  
Smooth Muscle ◽  
Muscle Activation ◽  
High Resistance State ◽  
Phase Iii ◽  
Extended Model ◽  
Stable States ◽  
Control Value ◽  
Model Predictions ◽  
Resistance State ◽  
Expired Gas

To evaluate the effect of increasing smooth muscle activation on the distribution of ventilation, lung impedance and expired gas concentrations were measured during a 16-breath He-washin maneuver in five nonasthmatic subjects at baseline and after each of three doses of aerosolized methacholine. Values of dynamic lung elastance (El,dyn), the curvature of washin plots, and the normalized slope of phase III ( S N) were obtained. At the highest dose, El,dyn was 2.6 times the control value and S N for the 16th breath was 0.65 liter−1. A previously described model of a constricted terminal airway was extended to include variable muscle activation, and the extended model was tested against these data. The model predicts that the constricted airway has two stable states. The impedances of the two stable states are independent of smooth muscle activation, but driving pressure and the number of airways in the high-resistance state increase with increasing muscle activation. Model predictions and experimental data agree well. We conclude that, as a result of the bistability of the terminal airways, the ventilation distribution in the constricted lung is bimodal.

Effects of norepinephrine on mechanics of arteries in vitro

1976 ◽  
Vol 231 (2) ◽  
pp. 420-425 ◽  
Author(s):  
RH Cox
Keyword(s):  
Smooth Muscle ◽  
Pressure Dependence ◽  
Muscle Activation ◽  
Characteristic Impedance ◽  
Transmural Pressure ◽  
External Diameter ◽  
Vascular Impedance ◽  
Before And After ◽  
Tonic Level

The effects of smooth muscle activation on the pressure dependence of arterial wall characteristic impedance were studied with isolated segments of canine iliac and carotid arteries. Measurements of external diameter and transmural pressure were made before and after activation of the arterial smooth muscle (SM) by norepinephrine (NE) in concentrations of 0.5 and 5 mug/ml and used to compute values of characteristic impedance (Z0). In the absence of SM tone, values of Z0 for both arterial sites increased monotonically with transmural pressure. For the larger [NE], values of ZO exhibited a minimum at pressures of the order of 125 mmHg and increased for both larger and smaller values of pressure, For the smaller [NE], values of Z0 showed a similar pressure dependence but with a broader minimum. It is concluded that the previously demonstrated constancy of vascular impedance with changes in arterial pressure is at least the result of the presence of a tonic level of SM activation in conduit arteries.

Saline infusion into lumen of resistance artery and small vein causes contraction

1990 ◽  
Vol 259 (1) ◽  
pp. H23-H28 ◽  
Author(s):  
J. A. Bevan ◽  
E. H. Joyce
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Physiological Saline ◽  
Saline Infusion ◽  
Resistance Artery ◽  
Resistance Arteries ◽  
Surface Receptors ◽  
Calcium Dependent ◽  
Rate Dependent ◽  
Physiological Saline Solution

Infusion of saline into the lumen of a resistance artery from the rabbit ear at rates between 0.5 and 20 microliters/min causes a rate-dependent maintained contraction. This contraction is independent of the direction of saline flow and of the endothelium. The contraction is prevented by pretreatment with the vasodilator papaverine (0.1 mM), which also reversed the contraction during flow. Exclusion of calcium from the physiological saline solution plus ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (1 mM) prevents the contraction, as does pre-exposure to cobalt (1 mM) and manganese (1 mM). Both these ions depress saline flow contraction once it is established. Saline flow-dependent contraction changes in a complex manner with temperature. It is greatest in resistance arteries from the pial, ear (skin), and femoral (muscle) segments, moderate to poor in coronary, mesenteric, and renal segments, and absent in the pulmonary segments. A small ear vein adjacent to the ear resistance artery also contracts to saline infusion. Although an explanation based on the washout of a vasodilator metabolite cannot be excluded, we favor the hypothesis that saline flow-induced shear stress of the inner surface of the vessel wall mechanically activates the vascular smooth muscle cells causing an extracellular Ca2(+)-dependent contraction. This response takes place through indomethacin-insensitive calcium-dependent mechanisms in vascular smooth muscle that differ from those associated with commonly studied surface receptors and with stretch.

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