Do α2-adrenergic agents modulate the effects of MIF-1 and Tyr-MIF-1 after three models of stress?

Effect of adrenergic agents on the secretion of gastrointestinal immunoreactive glucagon in depancreatized dogs

Diabetes ◽

10.2337/diabetes.29.5.355 ◽

1980 ◽

Vol 29 (5) ◽

pp. 355-360 ◽

Cited By ~ 2

Author(s):

T. Yoshida ◽

M. Kondo

Keyword(s):

Adrenergic Agents

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Induction And Potentiation Of Platelet Aggregation By Clonidine And 7ρ-Aminoclonidine, Partial Agonists Of The α2-Receptor Which Regulates Platelet Adenylate Cyclase

10.1055/s-0038-1652563 ◽

1981 ◽

Author(s):

David C Stump ◽

Donald E Macfarlane

Keyword(s):

Platelet Aggregation ◽

Cyclic Amp ◽

Adenylate Cyclase ◽

Specific Binding ◽

Phase 1 ◽

Intrinsic Activity ◽

Second Phase ◽

Adrenergic Agents ◽

Cyclic Amp Accumulation ◽

Induced Aggregation

Epinephrine induces platelet aggregation, potentiates aggregation by other agents, and blocks the stimulation of the adenylate cyclase by prostaglandins. Synthetic α-adrenergic agents have not been shown to induce aggregation. The effects of clonidine, an α2-agonist, and ρ-aminoclonidine on platelets were examined. Clonidine potentiated aggregation induced by 0.5μM ADP by 1.4-fold (1/2 max 0.5μM). It did not induce significant aggregation itself, and it inhibited aggregation induced by 5μM epinephrine (1/2 max lμM). It inhibited cyclic AMP accumulation induced by PGE1 by a maximum of 25% (1/2 max O.lμM) and it blocked inhibition by epinephrine. No significant specific binding of [3H] clonidine was observed to intact platelets. ρ-Aminoclonidine induced aggregation with delayed second phase (1/2 max 0.2μM), and potentiated ADP aggregation by 2-fold (1/2 max 0.2μM). Aggregation induced by epinephrine was more rapid, and was partially inhibited by ρ-aminoclonidine. It inhibited cyclic AMP accumulation by 50% max (1/2 max O.lμM) and attenuated epinephrine’s effect to the same level. The direct effects of ρ-aminoclonidine were blocked by lμM yohimbine, a selective α2-antagonist. Both clonidine and ρ—aminoclonidine blocked the specific binding of [3H]yohimbine (1/2 max 0.5μM). These results suggest that the platelet bears an α2-receptor with affinity for epinephrine, ρ-aminoclonidine and clonidine as agonists but that these agents display differing intrinsic activity and/or receptor reserve.

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Interactions between insulin and alpha 1-adrenergic agents in the regulation of glycogen metabolism in isolated hepatocytes.

Journal of Biological Chemistry ◽

10.1016/s0021-9258(18)88923-2 ◽

1985 ◽

Vol 260 (10) ◽

pp. 5963-5973 ◽

Cited By ~ 2

Author(s):

A P Thomas ◽

A Martin-Requero ◽

J R Williamson

Keyword(s):

Glycogen Metabolism ◽

Isolated Hepatocytes ◽

Adrenergic Agents

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Effects of endogenous and exogenous catecholamines on LPS-induced neutrophil trafficking and activation

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.1999.276.1.l1 ◽

1999 ◽

Vol 276 (1) ◽

pp. L1-L8 ◽

Cited By ~ 13

Author(s):

Edward Abraham ◽

Debra J. Kaneko ◽

Robert Shenkar

Keyword(s):

Systemic Circulation ◽

Mrna Levels ◽

Adrenergic Stimulation ◽

Neutrophil Accumulation ◽

Adrenergic Agonist ◽

Nitric Oxide Synthase Inhibitor ◽

Adrenergic Agents ◽

Adrenergic Antagonist ◽

Tnf Α ◽

Synthase Inhibitor

Endotoxemia produces elevations in catecholamine levels in the pulmonary and systemic circulation as well as rapid increases in neutrophil number and proinflammatory cytokine expression in the lungs. In the present experiments, we examined the effects of endogenous and exogenous adrenergic stimulation on endotoxin-induced lung neutrophil accumulation and activation. Levels of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and macrophage inflammatory protein (MIP)-2 mRNAs were increased in lung neutrophils from endotoxemic mice compared with those present in lung neutrophils from control mice or in peripheral blood neutrophils from endotoxemic or control mice. Treatment with the β-adrenergic antagonist propranolol before endotoxin administration did not affect trafficking of neutrophils to the lungs or the expression of IL-1β, TNF-α, or MIP-2 by lung neutrophils. Administration of the α-adrenergic antagonist phentolamine before endotoxemia did not alter lung neutrophil accumulation as measured by myeloperoxidase (MPO) levels but did result in significant increases in IL-1β, TNF-α, and MIP-2 mRNA expression by lung neutrophils compared with endotoxemia alone. Administration of the α1-adrenergic agonist phenylephrine before endotoxin did not affect trafficking of neutrophils to the lungs but was associated with significantly increased expression of TNF-α and MIP-2 mRNAs by lung neutrophils compared with that found after endotoxin alone. In contrast, treatment with the α2-adrenergic agonist UK-14304 prevented endotoxin-induced increases in lung MPO and lung neutrophil cytokine mRNA levels. The suppressive effects of UK-14304 on endotoxin-induced increases in lung MPO were not affected by administration of the nitric oxide synthase inhibitor N-nitro-l-arginine methyl ester. These data demonstrate that the initial accumulation and activation of neutrophils in the lungs after endotoxemia can be significantly diminished by α2-adrenergic stimulation. Therapy with α2-adrenergic agents may have a role in modulating inflammatory pulmonary processes associated with sepsis-induced acute lung injury.

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