Vascular Smooth Muscle, a Multiply Feedback-Coupled System of High Versatility, Modulation and Cell-Signaling Variability

1997 ◽  
Vol 17 (6) ◽  
pp. 360-373 ◽  
Author(s):  
G. Siegel ◽  
M. Malmsten ◽  
D. Klüssendorf ◽  
H.-W. Hofer
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Cell Signaling ◽  
Coupled System

Oxygen-dependent PAF receptor binding and intracellular signaling in ovine fetal pulmonary vascular smooth muscle

2005 ◽  
Vol 288 (5) ◽  
pp. L879-L886 ◽  
Author(s):  
Basil O. Ibe ◽  
Ada M. Portugal ◽  
Shiva Chaturvedi ◽  
J. Usha Raj
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Cell Signaling ◽  
Oxygen Tension ◽  
Intracellular Signaling ◽  
Platelet Activating Factor ◽  
Calcium Flux ◽  
Protein Synthesis Inhibitor ◽  
Synthesis Inhibitor ◽  
Paf Receptor

Circulating levels of platelet-activating factor (PAF) are high in the fetus, and PAF is active in maintaining high PVR in fetal hypoxia (Ibe BO, Hibler S, Raj J. J Appl Physiol 85: 1079–1085, 1998). PAF synthesis by fetal pulmonary vascular smooth muscle cells (PVSMC) is high in hypoxia, but how oxygen tension affects PAF receptor (PAF-r) binding in PVSMC is not known. We studied the effect of oxygen tension on PAF-r binding and signaling in fetal PVSMC. PAF binding was saturable. PAF-r density (Bmax: fmol/106 cells; means ± SE, n = 6), 25.2 ± 0.77 during hypoxia (Po2 <40 Torr), was higher than 13.9 ± 0.44 during normoxia (Po2 ∼100 Torr). Kd was twofold lower in hypoxia than normoxia. PAF-r protein expression, 35–40% greater in hypoxia, was inhibited by cycloheximide, a protein synthesis inhibitor, suggesting translational regulation. IP3 release, an index of PAF-r-mediated cell signaling, was greater in hypoxia (EC50: hypoxia, 2.94 ± 0.61; normoxia, 5.85 ± 0.51 nM). Exogenous PAF induced 50–90% greater intracellular calcium flux in cells during hypoxia, indicating hypoxia augments PAF-r-mediated cell signaling. PAF-r phosphorylation, with or without 5 nM PAF, was 40% greater in hypoxia. These data show 1) hypoxia upregulates PAF-r binding, PAF-r phosphorylation, and PAF-r-mediated intracellular signaling, evidenced by augmented IP3 production and intracellular Ca2+ flux; and 2) hypoxia-induced PAF-r phosphorylation results in activation of PAF-r-mediated signal transduction. The data suggest the fetal hypoxic environment facilitates PAF-r binding and signaling, thereby promoting PAF-mediated pulmonary vasoconstriction and maintenance of high PVR in utero.

Neuronal and Extraneuronal Uptake of 3H-Norepinephrine in the Heart of the Active Bat: An Electron Microscopic Radioautographic Study

1973 ◽  
Vol 31 ◽  
pp. 522-523
Author(s):  
Martin Hagopian ◽  
Michael D. Gershon ◽  
Eladio A. Nunez
Keyword(s):  
Smooth Muscle ◽  
Monoamine Oxidase ◽  
Vascular Smooth Muscle ◽  
Cardiac Muscle ◽  
Maximum Rate ◽  
External Medium ◽  
Extraneuronal Uptake ◽  
Electron Microscopic ◽  
Cardiac Tissues ◽  
High Affinity

The ability of cardiac tissues to take up norepinephrine from an external medium is well known. Two mechanisms, called Uptake and Uptake respectively by Iversen have been differentiated. Uptake is a high affinity system associated with adrenergic neuronal elements. Uptake is a low affinity system, with a higher maximum rate than that of Uptake. Uptake has been associated with extraneuronal tissues such as cardiac muscle, fibroblasts or vascular smooth muscle. At low perfusion concentrations of norepinephrine most of the amine taken up by Uptake is metabolized. In order to study the localization of sites of norepinephrine storage following its uptake in the active bat heart, tritiated norepinephrine (2.5 mCi; 0.064 mg) was given intravenously to 2 bats. Monoamine oxidase had been inhibited with pheniprazine (10 mg/kg) one hour previously to decrease metabolism of norepinephrine.

Sign in / Sign up

Export Citation Format

Share Document