Inhibition of noradrenaline release via presynaptic 5-HT1B receptors of the rat vena cava

1987 ◽  
Vol 336 (3) ◽  
Author(s):  
G.J. Molderings ◽  
K. Fink ◽  
E. Schlicker ◽  
M. G�thert
Keyword(s):  
Noradrenaline Release ◽  
Vena Cava ◽  
Rat Vena Cava

scholarly journals Noradrenaline release in the rat vena cava is inhibited by γ-aminobutyric acid via GABAB receptors but not affected by histamine

1991 ◽  
Vol 104 (2) ◽  
pp. 478-482 ◽  
Author(s):  
Dörthe Schneider ◽  
Eberhard Schlicker ◽  
Barbara Malinowska ◽  
Gerhard Molderings
Keyword(s):  
Noradrenaline Release ◽  
Vena Cava ◽  
Gabab Receptors ◽  
Aminobutyric Acid ◽  
Rat Vena Cava

CGP 35348 Blocks Noradrenaline- Release-Inhibiting GABAB Receptors in the Pig Retina, Rat Vena cava and Pithed Rat Vasculature

Pharmacology ◽  
1993 ◽  
Vol 47 (2) ◽  
pp. 111-116 ◽  
Author(s):  
Eberhard Schlicker ◽  
Barbara Malinowska ◽  
Markus Kathmann
Keyword(s):  
Noradrenaline Release ◽  
Vena Cava ◽  
Pithed Rat ◽  
Rat Vena Cava ◽  
Cgp 35348

Influence of spaceflight, hindlimb suspension, and venous occlusion on alpha 1-adrenoceptors in rat vena cava

1995 ◽  
Vol 78 (5) ◽  
pp. 1882-1888 ◽  
Author(s):  
I. Sayet ◽  
G. Neuilly ◽  
J. Mironneau ◽  
C. Mironneau
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Dissociation Constant ◽  
Binding Capacity ◽  
Vena Cava ◽  
Venous Occlusion ◽  
Hindlimb Suspension ◽  
Scatchard Analysis ◽  
Kinase C ◽  
Rat Vena Cava

Effects of hindlimb suspension, spaceflight, and venous occlusion were examined in isolated strips from rat vena cava by using both [3H]prazosin-binding and contraction responses evoked by norepinephrine. Sensitivity to norepinephrine was decreased without modification of the maximal contractile response. Furthermore, the high K(+)-induced contractions were not affected, suggesting that there was no interference with voltage-dependent Ca2+ channels. The sensitivity of the norepinephrine-induced contraction to prazosin was decreased, and Scatchard analysis of [3H]prazosin binding indicated an increase in the dissociation constant without variation in maximal binding capacity. A similar increase in the dissociation constant was obtained in control rats after pretreatment with 3 microM norepinephrine or 0.1 microM phorbol 12,13-dibutyrate to desensitize the protein kinase C. This effect was completely abolished in the presence of GF-109203X, a selective inhibitor of protein kinase C. Taken together, these data indicate that altered gravity conditions induce a desensitization of alpha 1B-adrenoceptors depending on increased protein kinase C activity. This effect can be mimicked by venous occlusion and may be responsible for reduced contractile responses to norepinephrine.

A model for passive elastic properties of rat vena cava

2007 ◽  
Vol 40 (14) ◽  
pp. 3130-3145 ◽  
Author(s):  
Georg Wolfgang Desch ◽  
Hans Werner Weizsäcker
Keyword(s):  
Elastic Properties ◽  
Vena Cava ◽  
Rat Vena Cava

Microfibrillar Elastic Polymer Wrapping of Rat Vena Cava for the Study of Engineered Arterial Vein Grafts

2010 ◽  
Author(s):  
Qiang Wang ◽  
Wei He ◽  
Yi Hong ◽  
William R. Wagner ◽  
David A. Vorp
Keyword(s):  
Saphenous Vein Graft ◽  
Vena Cava ◽  
Wall Stress ◽  
Cellular Injury ◽  
Vein Grafts ◽  
Ample Opportunity ◽  
Circumferential Wall Stress ◽  
Rat Vena Cava ◽  
Elastic Polymer ◽  
Polymer Wrapping

The autologous saphenous vein graft remains the graft of choice for 95% of surgeons performing coronary artery or peripheral bypass procedures. Within the first 5 years after implantation, 20%–40% of arterial vein grafts (AVG) fail due to intimal hyperplasia (IH)1. This adverse pathological response by AVGs may be in part due to their abrupt exposure to the significantly elevated circumferential wall stress associated with the arterial system2. We believe that if an AVG is given an ample opportunity to adapt and remodel to the stresses of the arterial environment, cellular injury may be reduced, thus limiting the initiating mechanisms of IH.

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