scholarly journals Cell Death–associated ADAMTS4 and Versican Degradation in Vascular Tissue

2009 ◽  
Vol 57 (9) ◽  
pp. 889-897 ◽  
Author(s):  
Richard D. Kenagy ◽  
Seung-Kee Min ◽  
Alexander W. Clowes ◽  
John D. Sandy
Keyword(s):  
Blood Flow ◽  
Cell Death ◽  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Fas Ligand ◽  
Vascular Tissue ◽  
Transcript Abundance ◽  
High Flow ◽  
The Other ◽  
Flow Through

High blood flow through baboon polytetrafluorethylene aorto-iliac grafts increases neointimal vascular smooth muscle cell (SMC) death, neointimal atrophy, and cleavage of versican to generate the DPEAAE neoepitope, a marker of ADAMTS-mediated proteolysis. In this study, we have determined the effect of high blood flow on transcript abundance in the neointima for ADAMTS1, −4, −5, −8, −9, −15, and −20. We found that after 24 hr of flow, the mRNA for ADAMTS4 was significantly increased, whereas that for the other family members was unchanged. Because vascular SMC death is markedly increased in the graft after 24 hr of high flow, we next examined the possibility that the ADAMTS4 induction and the cell death are causally related. The addition of Fas ligand to SMC cultures increased both ADAMTS4 mRNA and cell death ∼5-fold, consistent with the idea that ADAMTS4-dependent cleavage of versican may be partly responsible for cell death and tissue atrophy under these conditions.

scholarly journals Increased plasma angiotensin II in postural tachycardia syndrome (POTS) is related to reduced blood flow and blood volume

2006 ◽  
Vol 110 (2) ◽  
pp. 255-263 ◽  
Author(s):  
Julian M. Stewart ◽  
June L. Glover ◽  
Marvin S. Medow
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Blood Volume ◽  
High Flow ◽  
The Other ◽  
Low Flow ◽  
Postural Tachycardia Syndrome ◽  
Peripheral Blood Flow ◽  
Ang Ii ◽  
Postural Tachycardia

POTS (postural tachycardia syndrome) is associated with low blood volume and reduced renin and aldosterone; however, the role of Ang (angiotensin) II has not been investigated. Previous studies have suggested that a subset of POTS patients with increased vasoconstriction related to decreased bioavailable NO (nitric oxide) have decreased blood volume. Ang II reduces bioavailable NO and is integral to the renin–Ang system. Thus, in the present study, we investigated the relationship between blood volume, Ang II, renin, aldosterone and peripheral blood flow in POTS patients. POTS was diagnosed by 70° upright tilt, and supine calf blood flow, measured by venous occlusion plethysmography, was used to subgroup POTS patients. A total of 23 POTS patients were partitioned; ten with low blood flow, eight with normal flow and five with high flow. There were ten healthy volunteers. Blood volume was measured by dye dilution. All biochemical measurements were performed whilst supine. Blood volume was decreased in low-flow POTS (2.14±0.12 litres/m2) compared with controls (2.76±0.20 litres/m2), but not in the other subgroups. PRA (plasma renin activity) was decreased in low-flow POTS compared with controls (0.49±0.12 compared with 0.90±0.18 ng of Ang I·ml−1·h−1 respectively), whereas plasma Ang II was increased (89±20 compared with 32±4 ng/l), but not in the other subgroups. PRA correlated with aldosterone (r=+0.71) in all subjects. PRA correlated negatively with blood volume (r=−0.72) in normal- and high-flow POTS, but positively (r=+0.65) in low-flow POTS. PRA correlated positively with Ang II (r=+0.76) in normal- and high-flow POTS, but negatively (r=−0.83) in low-flow POTS. Blood volume was negatively correlated with Ang II (r=−0.66) in normal- and high-flow POTS and in five low-flow POTS patients. The remaining five low-flow POTS patients had reduced blood volume and increased Ang II which was not correlated with blood volume. The data suggest that plasma Ang II is increased in low-flow POTS patients with hypovolaemia, which may contribute to local blood flow dysregulation and reduced NO bioavailability.

scholarly journals Blood Perfusion of the Kidney of Lophius Piscatorius L.

1953 ◽  
Vol 32 (2) ◽  
pp. 329-336 ◽  
Author(s):  
L. Brull ◽  
E. Nizet ◽  
E. B. Verney
Keyword(s):  
Blood Flow ◽  
Critical Level ◽  
Perfusion Pressure ◽  
Blood Perfusion ◽  
Urine Flow ◽  
The Other ◽  
Protein Nitrogen ◽  
Other Hand ◽  
Flow Through

Lophius kidneys perfused with the heparinized blood (venous) of the fish secrete urine in which total non-protein nitrogen is concentrated, magnesium highly concentrated, and chloride only slightly so or not at all. Oxygenation of the blood, or lowering the temperature of the perfusate from c. 20° to c. 5° C. does not appear to influence secretion. The blood flow through the kidneys increases with the perfusion pressure, the increase often becoming disproportionately large. The urine flow, on the other hand, above a certain critical level is largely independent of changes in perfusion pressure.

scholarly journals A link between smooth muscle cell death and extracellular matrix degradation during vascular atrophy

2011 ◽  
Vol 54 (1) ◽  
pp. 182-191.e24 ◽  
Author(s):  
Richard D. Kenagy ◽  
Seung-Kee Min ◽  
Eileen Mulvihill ◽  
Alexander W. Clowes
Keyword(s):  
Extracellular Matrix ◽  
Cell Death ◽  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Matrix Degradation ◽  
Extracellular Matrix Degradation

scholarly journals Invasive Trophoblasts Stimulate Vascular Smooth Muscle Cell Apoptosis by a Fas Ligand-Dependent Mechanism

2006 ◽  
Vol 169 (5) ◽  
pp. 1863-1874 ◽  
Author(s):  
Lynda K. Harris ◽  
Rosemary J. Keogh ◽  
Mark Wareing ◽  
Philip N. Baker ◽  
Judith E. Cartwright ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell ◽  
Cell Apoptosis ◽  
Fas Ligand ◽  
Muscle Cell Apoptosis ◽  
Dependent Mechanism

scholarly journals Vascular smooth muscle cell death, autophagy and senescence in atherosclerosis

2018 ◽  
Vol 114 (4) ◽  
pp. 622-634 ◽  
Author(s):  
Mandy O J Grootaert ◽  
Manon Moulis ◽  
Lynn Roth ◽  
Wim Martinet ◽  
Cécile Vindis ◽  
...  
Keyword(s):  
Cell Death ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Vascular Smooth Muscle Cell

Microvascular dilation in response to occlusion: a coordinating role for conducted vasomotor responses

2000 ◽  
Vol 279 (1) ◽  
pp. H279-H284 ◽  
Author(s):  
Kim A. Dora ◽  
David N. Damon ◽  
Brian R. Duling
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Shear Stress ◽  
Smooth Muscle ◽  
Third Order ◽  
Vasomotor Responses ◽  
Vasodilatory Response ◽  
Flow Through ◽  
Stress Dependent ◽  
Dependent Mechanism

In rat cremasteric microcirculation, mechanical occlusion of one branch of an arteriolar bifurcation causes an increase in flow and vasodilation of the unoccluded daughter branch. This dilation has been attributed to the operation of a shear stress-dependent mechanism in the microcirculation. Instead of or in addition to this, we hypothesized that the dilation observed during occlusion is the result of a conducted signal originating distal to the occlusion. To test this hypothesis, we blocked the ascending spread of conducted vasomotor responses by damaging the smooth muscle and endothelial cells in a 200-μm segment of second- or third-order arterioles. We found that a conduction blockade eliminated or diminished the occlusion-associated increase in flow through the unoccluded branch and abolished or strongly attenuated the vasodilatory response in both vessels at the branch. We also noted that vasodilations induced by ACh (10−4 M, 0.6 s) spread to, but not beyond, the area of damage. Taken together, these data provide strong evidence that conducted vasomotor responses have an important role in coordinating blood flow in response to an arteriolar occlusion.

Fas/Fas ligand-mediated death pathway is involved in oxLDL-induced apoptosis in vascular smooth muscle cells

2001 ◽  
Vol 280 (3) ◽  
pp. C709-C718 ◽  
Author(s):  
Tzong-Shyuan Lee ◽  
Lee-Young Chau
Keyword(s):  
Cell Death ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Fas Ligand ◽  
Density Lipoprotein ◽  
Muscle Cells ◽  
Potent Inducer ◽  
Apoptotic Death

Oxidized low-density lipoprotein (oxLDL) is a potent inducer of apoptosis for vascular cells. In the present study, we demonstrate that the expression of death mediators, including p53, Fas, and Fas ligand (FasL) was substantially upregulated by oxLDL in cultured vascular smooth muscle cells (SMCs). The induction of these death mediators was time dependent and was accompanied by an increase in apoptotic death of SMCs following oxLDL treatment. Two oxysterols, 7β-hydroxycholesterol and 25-hydroxycholesterol, were also effective to induce the expression of death mediators and apoptosis. α-Tocopherol and deferoxamine significantly attenuated the induction of death mediators and cell death induced by oxLDL and oxysterols, suggesting that reactive oxygen species are involved in triggering the apoptotic event. Incubation of cells with FasL-neutralizing antibody inhibited the oxLDL-induced cell death up to 50%. Furthermore, caspase 8 and caspase 3 activities were induced time dependently in SMCs following oxLDL treatment. Collectively, these data suggest that the Fas/FasL death pathway is activated and responsible for, at least in part, the apoptotic death in vascular SMCs upon exposure to oxLDL.

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