Cyclic AMP accumulation in the beta adrenergic mechanism of eccrine sweat secretion

1981 ◽  
Vol 390 (1) ◽  
pp. 49-53 ◽  
Author(s):  
Kenzo Sato ◽  
Fusako Sato
Keyword(s):  
Cyclic Amp ◽  
Beta Adrenergic ◽  
Cyclic Amp Accumulation ◽  
Sweat Secretion ◽  
Adrenergic Mechanism ◽  
Eccrine Sweat

Cyclic AMP Second-Messenger Signal Amplification in Depression

1988 ◽  
Vol 152 (5) ◽  
pp. 665-669 ◽  
Author(s):  
Richard P. Ebstein ◽  
Bernard Lerer ◽  
Baruch Shapira ◽  
Zecharia Shemesh ◽  
Daniel G. Moscovich ◽  
...  
Keyword(s):  
Cyclic Amp ◽  
Signal Amplification ◽  
Antidepressant Treatment ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Late Night ◽  
Depressed Patients ◽  
Cyclic Amp Accumulation ◽  
Significant Clinical Improvement ◽  
Age And Sex

Beta-adrenergic-mediated cyclic AMP accumulation was reduced in lymphocytes obtained from depressed patients from that observed in an age- and sex-matched group of control subjects. Among the depressed patients, those not responding to treatment showed significantly lower pretreatment responses to isoproterenol compared with patients who exhibited significant clinical improvement during antidepressant treatment. Late-night (terminal) insomnia was significantly associated with the blunted response to beta-adrenergic stimulation. In depressed patients with the lowest isoproterenol response, the effect of forskolin (which acts distal to the receptor and directly stimulates the catalytic subunit) on cyclic AMP accumulation was also significantly decreased. This suggests that post-receptor modulations of signal amplification also play a role in the reduced response to beta-adrenergic stimulation in depression.

scholarly journals Effects of adrenalectomy on binding to and actions of adrenergic receptors

1986 ◽  
Vol 237 (2) ◽  
pp. 527-531 ◽  
Author(s):  
M F el-Refai ◽  
T M Chan
Keyword(s):  
Cyclic Amp ◽  
Binding Sites ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Glycogen Phosphorylase ◽  
Beta Adrenergic ◽  
Cyclic Amp Accumulation ◽  
Adrenergic Antagonists ◽  
Adrenergic Activation ◽  
Adrenalectomized Rats

Adrenalectomy results in significant changes in the mechanism of adrenergic activation of hepatic glycogenolysis. In adrenalectomized rats a greater role for the beta-adrenergic receptor is observed, whereas the alpha 1-adrenergic-mediated phosphorylase activation declines. Our present findings document that adrenalectomy causes a significant decrease in the high-affinity population of the alpha 1-adrenergic receptor labelled with [3H]adrenaline. Our data indicate a large increase in the number of beta-adrenergic binding sites after adrenalectomy. This increase was not consistent with the observed modest increase in the beta-adrenergic-mediated activation of cyclic AMP accumulation and glycogen phosphorylase. When alpha-adrenergic antagonists are present along with the catecholamine, a 100% increase in the adrenaline-mediated accumulation of cyclic AMP in hepatocytes from adrenalectomized rats was observed. Adrenalectomy was also shown to cause a significant increase in the hepatic alpha 2-adrenergic binding sites. These data are consistent with an inhibitory role on the beta-adrenergic-mediated activation of glycogenolysis by the hepatic alpha 2-adrenergic receptor in adrenalectomy.

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

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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