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Adrenergic Activation (adrenergic + activation)

Distribution by Scientific Domains

Medical Sciences	60%
Life Sciences	40%

Selected Abstracts

Psychosocial Stress Augments Tumor Development through ,-Adrenergic Activation in Mice

CANCER SCIENCE, Issue 7 2002
Hideo Hasegawa
Housing conditions affect behavioral and biological responses of animals. We investigated the effect of same-sex-grouped (G), crowded (GC) and isolated (I) conditions on the growth of B16 melanoma or Meth A fibrosarcoma implanted in the footpad of syngeneic male C57BL/6 or BALB/c mice. Differential housing altered host resistance to tumor growth. The host responses to stress were reflected in thymic atrophy, which was lowest in the G mice, highest in the GC mice and intermediate in the I mice. The GC condition was a more stressful social environment than the I condition in both male C57BL/6 and BALB/c mice. Reflecting the extent of psychosocial stress, tumor growth was augmented in the order of GC, I and G condition, and a negative mass correlation between tumor and thymus was observed, thus clearly indicating that the host resistance to tumors was attenuated by psychosocial stress. Furthermore, the stress-enhanced tumor growth and thymus atrophy were completely abrogated by the oral administration of the non-selective ,-adrenergic antagonist, propranolol. On the contrary, the chronic administration of corticosterone significantly induced the atrophy of thymus and spleen without affecting tumor growth. These results suggest an interrelationship among psychosocial stress, tumor growth and ,-adrenergic activation. [source]

Translation of striatal-enriched protein tyrosine phosphatase (STEP) after ,1-adrenergic receptor stimulation

JOURNAL OF NEUROCHEMISTRY, Issue 2 2007
Yaer Hu
Abstract The ,-adrenergic system is implicated in long-term synaptic plasticity in the CNS, a process that requires protein synthesis. To identify proteins that are translated in response to ,-adrenergic receptor stimulation and the pathways that regulate this process, we investigated the effects of isoproterenol on the translation of striatal-enriched protein tyrosine phosphatase (STEP) in both cortico-striatal slices and primary neuronal cultures. Isoproterenol stimulation induced a rapid dose-dependent increase in STEP expression. Anisomycin blocked the increase in STEP expression while actinomycin D had no effect, suggesting a translation-dependent mechanism. Isoproterenol-induced STEP translation required activation of ,1-receptors. Application of the MAPK/ERK kinase (MEK) inhibitor SL327 blocked both isoproterenol-induced activation of pERK and subsequent STEP translation. Inhibitors of PI3K (LY294002) or mTOR (rapamycin) also completely blocked STEP translation. These results suggest that co-activation of both the ERK and PI3K-Akt-mTOR pathways are required for STEP translation. As one of the substrates of STEP includes ERK itself, these results suggest that STEP is translated upon ,-adrenergic activation as part of a negative feedback mechanism. [source]

Regulation of In Situ Skeletal Muscle Arteriolar Tone: Interactions Between Two Parameters

MICROCIRCULATION, Issue 6 2002
JEFFERSON C. FRISBEEArticle first published online: 26 JAN 2010
ABSTRACT Objective: The growing understanding of the complexity of mechanisms regulating arteriolar tone demands that a systematic determination of how these processes interact to alter diameter be undertaken. This study examined how five mediators of skeletal muscle distal arteriolar tone [adenosine concentration, oxygen content, ,-adrenergic activation (norepinephrine), intravascular pressure and wall shear rate], taken two parameters at a time, interact to regulate vessel diameter. Methods: The reactivity of distal arterioles of in situ rat cremaster muscle after alterations in each of the above mediators was assessed. In addition, arteriolar responses to all two-parameter combinations were evaluated to determine the effect of altered environment on vascular reactivity to stimuli. Results: Arteriolar dilation to adenosine was unaltered by changes in other parameters. In contrast, wall shear rate-induced arteriolar dilation was impaired by 60,88% after increases in the other parameters. Myogenic reactivity was reduced by 28% with elevated O2 and by 65% with norepinephrine (because of vessel closure) and was impaired by 89% with elevated adenosine. O2 -induced arteriolar reactivity was impaired by 56% with increased adenosine and by 44% with increased norepinephrine concentration but was largely unaffected by elevated intravascular pressure. Adrenergic reactivity was attenuated with elevated intravascular pressure (by 69%) and O2 (by 54%) because of vessel closure but was unaltered with elevated adenosine. Conclusions: These data suggest that (1) individual mediators contributing to the regulation of arteriolar tone exist within a hierarchy of importance and (2) mechanisms regulating arteriolar tone can be impacted by unidentified alterations in other processes. Ongoing investigation into interactions between multiple processes regulating arteriolar tone will allow for a more integrated understanding of how microvessels regulate their diameter. [source]

,-Adrenergic inhibition increases collateral circuit conductance in rats following acute occlusion of the femoral artery

THE JOURNAL OF PHYSIOLOGY, Issue 6 2008
Jessica C. Taylor
This study evaluated whether ,-adrenergic activation contributes to collateral circuit vascular resistance in the hindlimb following acute unilateral occlusion of the femoral artery in rats. Blood pressures (BPs) were measured above (caudal artery) and below (distal femoral artery) the collateral circuit. Arterial BPs were reduced (15,35 mmHg) with individual (prazosin, rauwolscine) or combined (phentolamine) ,-receptor inhibition. Blood flows (BFs) were measured using microspheres before and after , inhibition during the same treadmill speed. ,1 inhibition increased blood flow by ,40% to active muscles that were not affected by femoral occlusion, whereas collateral-dependent BFs to the calf muscles were reduced by 29 ± 8.4% (P < 0.05), due to a decrease in muscle conductance with no change in collateral circuit conductance. ,2 inhibition decreased both collateral circuit (39 ± 6.0%; P < 0.05) and calf muscle conductance (36 ± 7.3%; P < 0.05), probably due to residual ,1 activation, since renal BF was markedly reduced with rauwolscine. Most importantly, inhibiting ,2 receptors in the presence of ,1 inhibition increased (43 ± 12%; P < 0.05) collateral circuit conductance. Similarly, non-selective , inhibition with phentolamine increased collateral conductance (242 ± 59%; P < 0.05). We interpret these findings to indicate that both ,1 - and ,2 -receptor activation can influence collateral circuit resistance in vivo during the high flow demands caused by exercise. Furthermore, we observed a reduced maximal conductances of active muscles that were ischaemic. Our findings imply that in the presence of excessive sympathetic activation, which can occur in the condition of intermittent claudication during exertion, an exaggerated vasoconstriction of the existing collateral circuit and active muscle will occur. [source]