scholarly journals Tyrosine Phosphorylation Modulates the Vascular Responses of Mesenteric Arteries from Human Colorectal Tumors

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Eduardo Ferrero ◽  
María Dolores Mauricio ◽  
Miriam Granado ◽  
Oscar García-Villar ◽  
Martín Aldasoro ◽  
...  
Keyword(s):  
Blood Flow ◽  
Tyrosine Phosphorylation ◽  
Isometric Tension ◽  
Mesenteric Arteries ◽  
Vegf Receptor ◽  
Organ Bath ◽  
Colorectal Tumors ◽  
Arterial Contraction ◽  
Normal Intestine ◽  
Stimulation Of

The aim of this study was to analyze whether tyrosine phosphorylation in tumoral arteries may modulate their vascular response. To do this, mesenteric arteries supplying blood flow to colorectal tumors or to normal intestine were obtained during surgery and prepared for isometric tension recording in an organ bath. Increasing tyrosine phosphorylation with the phosphatase inhibitor, sodium orthovanadate produced arterial contraction which was lower in tumoral than in control arteries, whereas it reduced the contraction to noradrenaline in tumoral but not in control arteries and reduced the relaxation to bradykinin in control but not in tumoral arteries. Protein expression of VEGF-A and of the VEGF receptor FLT1 was similar in control and tumoral arteries, but expression of the VEGF receptor KDR was increased in tumoral compared with control arteries. This suggests that tyrosine phosphorylation may produce inhibition of the contraction in tumoral mesenteric arteries, which may increase blood flow to the tumor when tyrosine phosphorylation is increased by stimulation of VEGF receptors.

scholarly journals in vitro Effects of Calcium Antagonists PN 200-110, Nifedipine, and Nimodipine on Human and Canine Cerebral Arteries

1983 ◽  
Vol 3 (3) ◽  
pp. 354-361 ◽  
Author(s):  
E. Müller-Schweinitzer ◽  
P. Neumann
Keyword(s):  
Rank Order ◽  
Cerebral Arteries ◽  
Isometric Tension ◽  
Mesenteric Arteries ◽  
Organ Bath ◽  
Vasoconstrictor Response ◽  
Dihydropyridine Derivative ◽  
Basilar Arteries ◽  
In Vitro Effects

PN 200–110 [4-(2, 1, 3-benzoxadiazol - 4 -) - 1,4-dihydro - 2,6 - dimethyl - pyridine - 3,5 - dicarboxylic acid methyl 1-methylethyl ester], a new dihydropyridine derivative, was investigated by recording isometric tension on spiral strips from human and canine arteries in tissue baths at 37°C. Responses to increasing concentrations of CaCl2 were investigated in calcium-free depolarizing solution (60 mmol/L KCl in equimolar replacement for NaCl, 50 mmol/L TRIZMA buffer, pH 7.4). Comparison of those concentrations that reduced the vasoconstrictor response to 1.6 mmol/L CaCl2 by 50% revealed the following order of potencies on both human and canine arteries: PN 200–110 > nimodipine > nifedipine. Responses to 5-hydroxytryptamine (5-HT) and blood were investigated in Krebs–Henseleit solution (NaHCO3 buffer). On canine arteries, PN 200–110 antagonized responses to 5-HT when used at 10–30 pmol/L; it was ∼70 times more potent on basilar than on mesenteric arteries, whereas both nifedipine and nimodipine were, respectively, ∼10 and 6 times more potent on basilar than on mesenteric arteries. When canine basilar arteries were constricted by the addition of blood to the organ bath, each of the investigated dihydropyridine derivatives elicited concentration-dependent relaxation, producing the following order of potencies: PN 200–110 > nifedipine = nimodipine. On human anterior cerebral arteries, the blood-induced contractions were counteracted in the following rank order: PN 200–110 = nimodipine > nifedipine. The results suggest that due to its potent calcium-blocking activity on cerebral arteries, PN 200–110 might be of value for the prevention and treatment of cerebrovascular spasms following subarachnoid hemorrhage.

scholarly journals Tyrosine phosphorylation of the vascular endothelial-growth-factor receptor-2 (VEGFR-2) is modulated by Rho proteins

2000 ◽  
Vol 348 (2) ◽  
pp. 273-280 ◽  
Author(s):  
Denis GINGRAS ◽  
Sylvie LAMY ◽  
Richard BÉLIVEAU
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Tyrosine Phosphorylation ◽  
Growth Factor Receptor ◽  
Vegf Receptor ◽  
Vascular Endothelial ◽  
Rho Proteins ◽  
Transient Overexpression ◽  
Endothelial Growth Factor ◽  
Stimulation Of

The effects of Rho-specific modifying toxins on the tyrosine phosphorylation of endothelial cell proteins were investigated. Incubation of the cells with the Rho-activating toxin cytotoxic necrotizing factor 1 (CNF1) induced a marked increase in the tyrosine phosphorylation of a number of signalling intermediates of the vascular endothelial growth factor (VEGF)-mediated cascade, including focal adhesion kinase, paxillin, phospholipase Cγ1 and a Shc-associated protein of 195 kDa. Both CNF1- and VEGF-dependent tyrosine phosphorylation of these proteins were significantly reduced by prior incubation with C3 transferase, a known inhibitor of RhoA function, suggesting a Rho-dependent mechanism. The stimulation of endothelial cells with CNF1 resulted in a marked increase in the tyrosine phosphorylation of the VEGF receptor (VEGFR)-2, which was correlated with a stimulation of its kinase activity and with its association with downstream tyrosine phosphorylated proteins. The stimulatory effect of CNF1 was specific for VEGFR-2 since the phosphotyrosine content of VEGFR-1 was not affected by the toxin. Transient overexpression of a dominant-active RhoA mutant also induced an increase in the tyrosine phosphorylation of the VEGFR-2, whereas overexpression of a dominant-inactive form of the protein was without effect. Taken together, these results indicate that Rho proteins may play an important role in angiogenesis by modulating the tyrosine phosphorylation levels of VEGFR-2.

Induction of matrix metalloproteinase-2 enhances systemic arterial contraction after hypoxia

2007 ◽  
Vol 292 (1) ◽  
pp. H684-H693 ◽  
Author(s):  
Jeff Z. He ◽  
Adrian Quan ◽  
Yi Xu ◽  
Hwee Teoh ◽  
Guilin Wang ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Systemic Circulation ◽  
Mesenteric Arteries ◽  
Matrix Metalloproteinase 2 ◽  
Organ Bath ◽  
Mrna Levels ◽  
Resistance Arteries ◽  
Protein Levels ◽  
Arterial Contraction ◽  
Membrane Type

This study was carried out to determine the role of increased vascular matrix metalloproteinase-2 (MMP-2) expression in the changes in systemic arterial contraction after prolonged hypoxia. Rats and mice were exposed to hypoxia (10% and 8% O2, respectively) or normoxia (21% O2) for 16 h, 48 h, or 7 days. Aortae and mesenteric arteries were either mounted in organ bath myographs or frozen in liquid nitrogen. MMP-2 inhibition with cyclic CTTHWGFTLC (CTT) reduced contraction to phenylephrine (PE) in aortae and mesenteric arteries from rats exposed to hypoxia for 7 days but not in vessels from normoxic rats. Similarly, CTT reduced contraction to Big endothelin-1 (Big ET-1) in aortae from rats exposed to hypoxia for 7 days. Responses to PE were reduced in hypoxic MMP-2−/− mice compared with MMP-2+/+ mice. Increased contraction to Big ET-1 after hypoxia was observed in MMP-2+/+ mice but not in MMP-2−/− mice. Rat aortic MMP-2 and membrane type 1 (MT1)-MMP protein levels and MMP activity were increased after 7 days of hypoxia. Rat aortic MMP-2 and MT1-MMP mRNA levels were increased in the deep medial vascular smooth muscle. We conclude that hypoxic induction of MMP-2 expression potentiates contraction in systemic conduit and resistance arteries. This may preserve the capacity to regulate the systemic circulation in the transition between the alterations in vascular tone and structural remodeling that occurs during prolonged hypoxic epochs.

Tension response of mammalian muscle to intra-arterial acetylcholine

1960 ◽  
Vol 198 (3) ◽  
pp. 507-510 ◽  
Author(s):  
Peter T. Rowley ◽  
Jay B. Wells ◽  
Richard L. Irwin
Keyword(s):  
Dose Response ◽  
Contractile Response ◽  
Tibialis Anterior Muscle ◽  
Arterial Occlusion ◽  
Isometric Tension ◽  
Neural Stimulation ◽  
Dose Response Relationship ◽  
Mammalian Muscle ◽  
Tension Response ◽  
Stimulation Of

Using isometric tension recording of the tibialis anterior muscle of the cat, the response to intra-arterial acetylcholine injection was studied and compared to the response to electrical stimulation of the nerve. The amount of acetylcholine, the rate of injection and the volume of diluent injected are interrelated factors in the production of tension. Regardless of the amount and concentration of the acetylcholine injected, the contractile response of the muscle has a slower rate of rise and a longer duration than the response from single maximal impulse stimulation to the nerve and a maximal tension less than from a tetanic neural stimulation. The dose-response relationship between the injected acetylcholine and the resultant tension and its modification by curare are described. The steep portion of the dose-response curve was found to occur in most experiments between 0.5 and 6.0 µg. A method of supplying blood to the muscle is described which provides more reliable intermittent arterial occlusion during injection.

Effects of Electrical Stimulation of the Superior Cervical Ganglion on Cochlear Blood Flow in Guinea Pig

1993 ◽  
Vol 113 (2) ◽  
pp. 146-151 ◽  
Author(s):  
Tian-Ying Ren ◽  
E. Laurikainen ◽  
W. S. Quirk ◽  
J. M. Miller ◽  
A. L. Nuttall
Keyword(s):  
Blood Flow ◽  
Electrical Stimulation ◽  
Guinea Pig ◽  
Superior Cervical Ganglion ◽  
Cochlear Blood Flow ◽  
Cervical Ganglion ◽  
Stimulation Of
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