Numerical analyses of the interrelation between extracellular smooth muscle orientation and intracellular filament overlap in the human abdominal aorta

Investigation of the effect of α1-adrenergic receptor subtypes on the contraction of the abdominal aorta will allow for more effective treatment of hypertension by use of selective antagonists. The aim of the study was to evaluate the participation of α1-adrenergic receptor subtypes in the contractility of the aortic smooth muscle cells in rabbits. The in vitro experiments were performed in isolated tissue preparations from 30 adult female New Zealand rabbits. The abdominal aortic sections were placed in organ bath chambers and contracted with increasing doses of non-selective α1-adrenergic receptor agonist phenylephrine without pre-incubation or after incubation in α1-adrenergic receptor subtype-selective or non-selective antagonists. Separate sections were incubated with increasing concentrations of antagonists. Phenylephrine caused maximal rise in arterial smooth muscle tone to 4.75 ± 0.47 mN. The most potent in blocking phenylephrine induced contraction was 5-metylurapidil (α1A-adrenergic receptor antagonist) followed by phentolamine and prazosin (non-selective α1-adrenergic receptor antagonists); BMY 7378 (α1D-adrenergic receptor antagonist), cyclazosin and L-765.314 (α1B-adrenergic receptor antagonists) were less effective. All antagonists, except BMY 7378 elicited relaxation of non-precontracted aorta in dose dependent manner. Our results indicate that postsynaptic α1A receptors are the most potent in producing rabbit abdominal aorta contraction, while α1B and α1D subtypes are less effective.

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Abdominal Aortic Healing Associated with a Thin-Walled Dacron—Covered Endovascular Graft in a Canine Model

Journal of Endovascular Therapy ◽

10.1177/152660280200900312 ◽

2002 ◽

Vol 9 (3) ◽

pp. 333-343 ◽

Cited By ~ 6

Author(s):

Donny B. Dal Ponte ◽

Scott S. Berman ◽

Vangie Patula ◽

Leigh Kleinert ◽

Stuart K. Williams

Keyword(s):

Smooth Muscle ◽

Abdominal Aorta ◽

Vessel Wall ◽

Canine Model ◽

Graft Material ◽

Luminal Surface ◽

Endovascular Graft ◽

Smooth Flow ◽

Healing Response ◽

Subendothelial Space

Purpose: To characterize the healing response associated with an experimental endovascular graft (EVG) by examining the lumen of the prosthesis and the native vessel wall responses after implantation in a canine model. Methods: An endovascular graft (EVG) constructed of hookless self-expanding nitinol springs covered by an ultrathin Dacron fabric was placed in the abdominal aorta of 8 dogs following femoral artery catheterization. After 12 weeks, specimens were subjected to histological and immunocytochemical testing to quantitatively and qualitatively analyze the cellular makeup of the luminal and abluminal tissues. Results: Gross examination revealed a glistening, thrombus-free luminal surface on all prostheses, which was confirmed by scanning electron microscopy. The EVGs were well incorporated into the aortic wall, leaving a concentric, smooth flow surface. Immunocytochemistry-verified the presence of von Willebrand factor—positive endothelial cells on the luminal surface and α-smooth muscle cell actin—positive smooth muscle and/or fibroblast cells in the subendothelial space. A sparse inflammatory response and a paucity of proliferating nuclear cell antigen—positive cells were noted within the neomedial lining adjacent to the graft material. In addition, a rich vaso vasorum—like plexus of microvessels was evident within the neomedial tissue. The native vessel wall upon which the EVG impinged was largely unaffected. Conclusions: These data demonstrate that placement of an experimental EVG in the canine abdominal aorta elicits a healing response that is distinct from interpositional vascular grafts. Results from this study have particular relevance to the proximal and distal anastomotic neck regions.

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Abstract P281: Vascular Remodeling And Impaired Vascular Smooth Muscle Cell Plasticity In Age And Sex-dependent Hypertension

Hypertension ◽

10.1161/hyp.78.suppl_1.p281 ◽

2021 ◽

Vol 78 (Suppl_1) ◽

Author(s):

Razie Amraei ◽

Kayla Nist ◽

Jesse Moreira ◽

Richard D Wainford

Keyword(s):

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Smooth Muscle Cell ◽

Abdominal Aorta ◽

Vascular Remodeling ◽

Vascular Dysfunction ◽

Renal Arteries ◽

Cell Plasticity ◽

Sd Rats ◽

Age And Sex

Aim: Hypertension (HTN) and aging are associated with the development of vascular dysfunction. We speculated that vascular smooth muscle cell plasticity and vascular remodeling play major roles in age and sex-dependent HTN. Methods: Male and female Sprague-Dawley (SD) rats aged 3 and 16-months-old (N=6/group) were housed under standard conditions. Blood pressure was measured via femoral artery cannulation and sympathetic tone to the vasculature was estimated by ganglion blockade via Hexamethonium (30mg/Kg IV). PBS-perfused abdominal aorta and renal arteries were collected and immunoblotting was performed following protein extraction. Results: Male SD rats, but not females, develop HTN and increased sympathetic tone with age. Aged hypertensive male rats, but not aged normotensive females, exhibit reduced p-Erk1/2 and p-eNos levels in both abdominal aorta and renal arteries. α-Smooth Muscle Actin significantly increased in aged male abdominal aorta. Elevated c-Src was observed in aged female abdominal aorta and p-c-Src was reduced in aged male abdominal aorta. Caveolin-1 changed oppositely in young and aged abdominal aorta and renal arteries of two sexes. Conclusions: Our data suggest that artery-specific changes of key signaling molecules contribute to impaired vascular smooth muscle plasticity and vascular dysfunction in aged hypertensive male but not in aged normotensive female rats.

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Aneurysmal and occlusive atherosclerosis of the human abdominal aorta

Journal of Vascular Surgery ◽

10.1016/0741-5214(93)90274-p ◽

1993 ◽

Vol 18 (3) ◽

pp. 526

Keyword(s):

Abdominal Aorta ◽

Human Abdominal Aorta

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Platelet And Smooth Muscle Cell Responses After Endothelial Desquamation

10.1055/s-0038-1652729 ◽

1981 ◽

Author(s):

M B Stemerman

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Abdominal Aorta ◽

Vessel Wall ◽

Balloon Catheter ◽

Muscle Cells ◽

Mechanical Removal ◽

Cell Counts ◽

Old Rats

Although compromise of endothelial integrity occurs through many mechanisms, mechanical removal by balloon catheter is an excellent experimental method to study vascular responsiveness after injury. The interaction of platelets with the vessel wall, as well as proliferation of vascular smooth muscle cells can be assessed in this model. Following platelet attachment to the subendothelium, platelets release materials from their alpha granules. Using an antibody raised against platelet factor 4, a protein stored in alpha granules, we have demonstrated that material released from platelets do enter the vessel wall. A large amount of PF 4 antigen enters the wall shortly after endothelial removal, permeating the wall completely by 30 minutes, but little trace of the antigen can be found four hours after injury. Using infusions of PGI2 to a level of 850 ng/kg/min in rabbits, in vivo platelet adhesion to the exposed subendothelium can be greatly reduced and release of PF4 antigen into the vessel wall markedly diminished. Growth of smooth muscle cells (SMC) after endothelial removal has also been measured by 3H-Thymidine labeling of SMC DNA. As measured by this method as well as direct cell counts, SMC proliferation in the abdominal aorta is significantly greater than the thoracic. Reinjury of only the abdominal aorta by balloon catheter 4 days after the initial total aortic injury causes a proliferative spurt in the thoracic aortic SMC, thus demonstrating that a humoral signal can initiate SMC proliferation. In addition, the response of SMC from 21 month old rats when compared with 3 month old rats is much greater. These studies demonstrate in vivo methods for examining the response of platelets and SMC following endothelial injury. Further, these studies indicate that the response to injury hypothesis of atherosclerosis progression should now be broadened to the concept of a response to signal view of atherogenesis.

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Velocity profiles in the normal human abdominal aorta: A comparison between ultrasound and magnetic resonance data

Ultrasound in Medicine & Biology ◽

10.1016/0301-5629(89)90160-9 ◽

1989 ◽

Vol 15 (2) ◽

pp. 113-119 ◽

Cited By ~ 13

Author(s):

A. Vieli ◽

U. Moser ◽

S. Maier ◽

D. Meier ◽

P. Boesiger

Keyword(s):

Magnetic Resonance ◽

Abdominal Aorta ◽

Velocity Profiles ◽

Magnetic Resonance Data ◽

Resonance Data ◽

Normal Human ◽

Human Abdominal Aorta

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Layer- and Direction-Specific Material Properties, Extreme Extensibility and Ultimate Material Strength of Human Abdominal Aorta and Aneurysm: A Uniaxial Extension Study

Annals of Biomedical Engineering ◽

10.1007/s10439-015-1323-6 ◽

2015 ◽

Vol 43 (11) ◽

pp. 2745-2759 ◽

Cited By ~ 17

Author(s):

Zhongzhao Teng ◽

Jiaxuan Feng ◽

Yongxue Zhang ◽

Yuan Huang ◽

Michael P. F. Sutcliffe ◽

...

Keyword(s):

Abdominal Aorta ◽

Material Properties ◽

Uniaxial Extension ◽

Extension Study ◽

Material Strength ◽

Specific Material ◽

Human Abdominal Aorta

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TGF-β (Transforming Growth Factor-β) Signaling Protects the Thoracic and Abdominal Aorta From Angiotensin II-Induced Pathology by Distinct Mechanisms

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvbaha.117.309401 ◽

2017 ◽

Vol 37 (11) ◽

pp. 2102-2113 ◽

Cited By ~ 33

Author(s):

Stoyan N. Angelov ◽

Jie Hong Hu ◽

Hao Wei ◽

Nathan Airhart ◽

Minghui Shi ◽

...

Keyword(s):

Smooth Muscle ◽

Angiotensin Ii ◽

Growth Factor ◽

Abdominal Aorta ◽

Neutralizing Antibodies ◽

Transforming Growth Factor ◽

Transforming Growth Factor Β ◽

Specific Loss ◽

Aortic Pathology ◽

Thoracic And Abdominal

Objective— The role of TGF-β (transforming growth factor-β) signaling in abdominal aortic aneurysm (AAA) formation is controversial. Others reported that systemic blockade of TGF-β by neutralizing antibodies accelerated AAA development in angiotensin II-infused mice. This result is consistent with other studies suggesting that TGF-β signaling prevents AAA. Development of a therapy for AAA that exploits the protective actions of TGF-β would be facilitated by identification of the mechanisms through which TGF-β prevents AAA. We hypothesized that TGF-β signaling prevents AAA by its actions on aortic medial smooth muscle cells. Approach and Results— We compared the prevalence, severity, and histopathology of angiotensin II-induced AAA among control mice (no TGF-β blockade), mice with antibody-mediated systemic neutralization of TGF-β, and mice with genetically based smooth muscle–specific loss of TGF-β signaling. Surprisingly, we found that systemic—but not smooth muscle–specific—TGF-β blockade significantly increased the prevalence of AAA and tended to increase AAA severity, adventitial thickening, and aortic wall macrophage accumulation. In contrast, abdominal aortas of mice with smooth muscle–specific loss of TGF-β signaling differed from controls only in having a thinner media. We examined thoracic aortas of the same mice. Here we found that smooth muscle–specific loss of Tgfbr2 —but not systemic TGF-β neutralization—significantly accelerated development of aortic pathology, including increased prevalence of intramural hematomas, medial thinning, and adventitial thickening. Conclusion— Our results suggest that TGF-β signaling prevents both abdominal and thoracic aneurysmal disease but does so by distinct mechanisms. Smooth muscle extrinsic signaling protects the abdominal aorta and smooth muscle intrinsic signaling protects the thoracic aorta.

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