Interaction of β-adrenergic agonists and antagonists with the stimulation of growth hormone release induced by clonidine or by morphine in the rat

1982 ◽  
Vol 94 (3) ◽  
pp. 327-331 ◽  
Author(s):  
M. T. Bluet-Pajot ◽  
D. Durand ◽  
F. Mounier ◽  
C. Schaub ◽  
C. Kordon
Keyword(s):  
Adrenergic Receptors ◽  
Hormone Release ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Basal Secretion ◽  
Experimental Conditions ◽  
Gamma Hydroxybutyrate ◽  
Β Adrenergic Receptors ◽  
Dose Dependent

The β-adrenergic agonist, isoprenaline, and antagonist, propranolol, had no effect on the delayed basal secretion of GH consistently observed in rats treated with the narco-analgesic gamma-hydroxybutyrate. Under the same experimental conditions, GH release was distinctly stimulated by infusion of the α-adrenergic agonist, clonidine, and by morphine; both responses were dose-dependent. The effects of β-adrenergic agonists and antagonists on these GH responses were as follows: in rats pretreated with isoprenaline the GH release induced by clonidine and morphine was abolished whereas it was enhanced in rats pretreated with propranolol. These data confirmed and extended previous reports from this laboratory on the inhibitory role of β-adrenergic receptors on GH regulation.

scholarly journals Expression of adrenergic receptors in mouse preimplantation embryos and ovulated oocytes

Reproduction ◽  
2007 ◽  
Vol 133 (6) ◽  
pp. 1139-1147 ◽  
Author(s):  
Štefan Čikoš ◽  
Pavol Rehák ◽  
Soňa Czikková ◽  
Jarmila Veselá ◽  
Juraj Koppel
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Cell Number ◽  
Embryo Cell ◽  
Preimplantation Embryos ◽  
Adrenergic Agonist ◽  
And Migration ◽  
Β Adrenergic Receptors ◽  
Dose Dependent ◽  
Receptor Family

Epinephrine and norepinephrine can play an important role in basic developmental processes such as embryogenesis and morphogenesis, regulating cell proliferation, differentiation and migration. We showed that β-adrenergic receptors can mediate the effects of catecholamines on preimplantation embryos in our previous work. In the present study, we designed specific oligonucleotide primers which can distinguish among all members of the α-adrenergic receptor family, and showed (using RT-PCR) that the α2C-adrenergic receptor is transcribed in ovulated oocytes, 8- to 16-cell morulae and expanded blastocysts. We did not detect the α2C-adrenoceptor transcript in 4-cell embryos. Our immunohistochemical study showed the presence of α-2C-adrenoceptor protein in ovulated oocytes, 8- to 16- cell embryos and blastocysts, but the signal in 4-cell embryos was weak, and probably represents remaining protein of maternal origin. We did not detect any other α-adrenergic receptor in preimplantation embryos and oocytes. Exposure of mouse preimplantation embryos to the α2-adrenergic agonist UK 14 304 led to significant reduction of the embryo cell number, and the effect was dose dependent. Our results suggest that epinephrine and norepinephrine could affect the embryo development in the oviduct via adrenergic receptors directly and support the opinion that maternal stress can influence the embryo even in very early pregnancy.

scholarly journals Role of β-Adrenergic Receptors and Nitric Oxide Signaling in Exercise-Mediated Cardioprotection

Physiology ◽  
2013 ◽  
Vol 28 (4) ◽  
pp. 216-224 ◽  
Author(s):  
John W. Calvert ◽  
David J. Lefer
Keyword(s):  
Nitric Oxide ◽  
Risk Factors ◽  
Adrenergic Receptors ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nitric Oxide Signaling ◽  
Factors Associated ◽  
Cardioprotective Effects ◽  
Β Adrenergic Receptors

Exercise promotes cardioprotection in both humans and animals not only by reducing risk factors associated with cardiovascular disease but by reducing myocardial infarction and improving survival following ischemia. This article will define the role that nitric oxide and β-adrenergic receptors play in mediating the cardioprotective effects of exercise in the setting of ischemia-reperfusion injury.

scholarly journals Adrenergic and Cholinergic Receptors of Cerebral Microvessels

1981 ◽  
Vol 1 (3) ◽  
pp. 329-338 ◽  
Author(s):  
Sami I. Harik ◽  
Virendra K. Sharma ◽  
John R. Wetherbee ◽  
Robert H. Warren ◽  
Shailesh P. Banerjee
Keyword(s):  
Adrenergic Receptors ◽  
Specific Binding ◽  
Cholinergic Receptors ◽  
Biologically Active ◽  
Adrenergic Agonists ◽  
Muscarinic Cholinergic Receptors ◽  
Cerebral Microvessels ◽  
Binding Characteristics ◽  
Muscarinic Cholinergic ◽  
Β Adrenergic Receptors

The presence of α- and β-adrenergic and muscarinic cholinergic receptors in cerebral microvessels of the rat and pig was assessed by ligand binding techniques. The results demonstrate the presence of specific binding to α2- and β-adrenergic receptors but no appreciable specific binding to α1-adrenergic or muscarinic cholinergic receptors. β-Adrenergic receptors of pig cerebral microvessels are similar to those of the brain and other organs in their binding characteristics to the tritiated ligand and in their stereospecificity of binding to the biologically active isomers of β-adrenergic agonists. Further evidence derived from the differential potency of binding displacement by the various β-adrenergic agonists and selective β1- and β2-adrenergic antagonists indicates that β-adrenergic receptors of pig cerebral microvessels are mostly of the β2-subtype.

scholarly journals Adrenergic Regulation of Macrophage-Mediated Innate/Inflammatory Responses in Obesity and Exercise in this Condition: Role of β2 Adrenergic Receptors

2019 ◽  
Vol 19 (8) ◽  
pp. 1089-1099 ◽  
Author(s):  
Eduardo Ortega ◽  
Isabel Gálvez ◽  
Leticia Martín-Cordero
Keyword(s):  
Stress Responses ◽  
Adrenergic Receptors ◽  
Inflammatory Responses ◽  
Low Grade ◽  
Adrenergic Stimulation ◽  
Adrenergic Regulation ◽  
Induce Insulin Resistance ◽  
Antiinflammatory Effects ◽  
Β Adrenergic Receptors

Background: The effects of exercise on the innate/inflammatory immune responses are crucially mediated by catecholamines and adrenoreceptors; and mediations in both stimulatory and anti-inflammatory responses have been attributed to them. Obesity and metabolic syndrome are included among low-grade chronic inflammatory pathologies; particularly because patients have a dysregulation of the inflammatory and stress responses, which can lead to high levels of inflammatory cytokines that induce insulin resistance, contributing to the onset or exacerbation of type 2 diabetes. Macrophages play a crucial role in this obesity-induced inflammation. Although most of the antiinflammatory effects of catecholamines are mediated by β adrenergic receptors (particularly β2), it is not known whether in altered homeostatic conditions, such as obesity and during exercise, innate/ inflammatory responses of macrophages to β2 adrenergic stimulation are similar to those in cells of healthy organisms at baseline. Objective: This review aims to emphasize that there could be possible different responses to β2 adrenergic stimulation in obesity, and exercise in this condition. Methods: A revision of the literature based on the hypothesis that obesity affects β2 adrenergic regulation of macrophage-mediated innate/inflammatory responses, as well as the effect of exercise in this context. Conclusion: The inflammatory responses mediated by β2 adrenoreceptors are different in obese individuals with altered inflammatory states at baseline compared to healthy individuals, and exercise can also interfere with these responses. Nevertheless, it is clearly necessary to develop more studies that contribute to widening the knowledge of the neuroimmune regulation process in obesity, particularly in this context.

Hypothalamic α-adrenergic blockade modifies drinking and blood pressure responses to central angiotensin II in conscious rats

1988 ◽  
Vol 66 (10) ◽  
pp. 1270-1277 ◽  
Author(s):  
D. L. Jones
Keyword(s):  
Angiotensin Ii ◽  
Adrenergic Receptors ◽  
Adrenergic Blockade ◽  
Drinking Response ◽  
Pressor Responses ◽  
Awake Rat ◽  
Rostral Hypothalamus ◽  
Blood Pressure Responses ◽  
Β Adrenergic Receptors ◽  
Dose Dependent

These experiments investigated in the awake rat the involvement of noradrenergic projections to the rostral hypothalamus in the drinking and pressor responses elicited by intracerebroventricular (i.c.v.) injections of 25 ng of angiotensin II. Phentolamine mesylate in doses of 2.5–125 μg injected into the rostral hypothalamus produced a dose-dependent depression of both the drinking and pressor responses elicited by i.c.v. administration of angiotensin II. A paradoxical increase in heart rate was associated with a decrease in pressor responses with increasing doses of phentolamine. This response was due to tissue injections, since pretreatment by injecting 12.5 μg of phentolamine into the ventricle did not block either the cardiovascular or drinking responses to i.c.v. injections of angiotensin II. Yohimbine (0.33–3.3 μg), DL-propranolol (25 μg), and atenolol (25 μg) did not, but prazosin (0.7 μg) did significantly alter the pressor responses. Although yohimbine also was without effect on drinking, prazosin reduced the drinking responses. These results suggest that α1-adrenergic receptors in the rostral hypothalamus are involved in the control of both the drinking and pressor responses elicited by i.c.v. injections of angiotensin II. In the case of propranolol and atenolol, β-adrenergic receptors altered only the drinking response in a nonspecific manner by eliciting competing behaviors. Whether they are involved in modifying the drinking response only remains to be demonstrated.

Characterization of myometrial desensitization to β-adrenergic agonists

1990 ◽  
Vol 68 (10) ◽  
pp. 1377-1384 ◽  
Author(s):  
Brian A. Dayes ◽  
Stephen J. Lye
Keyword(s):  
Adrenergic Receptors ◽  
Contractile Activity ◽  
Significant Inhibition ◽  
Scatchard Analysis ◽  
Continuous Exposure ◽  
Partial Recovery ◽  
Adrenergic Agonists ◽  
Camp Content ◽  
Adrenoceptor Antagonist ◽  
Β Adrenergic Receptors

Continuous exposure of ovine myometrial strips exposed to isoproterenol (10 μM) resulted in only transient inhibition with contractions returning within 60 min. Rechallenging these strips with isoproterenol failed to induce inhibition, confirming the occurrence of desensitization. In contrast, exposure of myometrial tissue to isoproterenol for only 5 min did not result in desensitization. Myometrial strips exposed to isoproterenol demonstrated a significant increase in cAMP content associated with inhibition of contractile activity and a subsequent fall in cAMP content upon desensitization. Elevation of endogenous cAMP levels by either inhibition of cAMP-dependent phosphodiesterase activity (0.5 mM isobutylmethylxanthine, in ovine strips) or direct activation of adenylyl cyclase (10 μM forskolin, in rat strips) induced a rapid and significant inhibition of myometrial contractile activity in desensitized tissue. Scatchard analysis of the binding of the β-adrenoceptor antagonist, [125I]iodocyanopindolol, revealed a significant reduction in the concentration of β-adrenergic receptors (but no change in binding affinity) in desensitized myometrial tissue. Incubation of desensitized tissue with fresh buffer for 3 h induced only a partial recovery in responsiveness to isoproterenol. These data suggest that prolonged, but not acute, exposure of the myometrium to β-adrenergic agonists induces a state of desensitization that is associated with a down-regulation of β-adrenoceptors but maintenance of postreceptor function.Key words: myometrium, contraction, β-adrenergic receptors, β-antagonists.

β-Adrenergic induced K + current in Xenopus oocytes: role of cAMP, inhibition by muscarinic agents

1985 ◽  
Vol 223 (1232) ◽  
pp. 389-402 ◽  
Keyword(s):  
Adenylate Cyclase ◽  
Adrenergic Receptors ◽  
Xenopus Oocytes ◽  
Follicular Cells ◽  
K Current ◽  
Β Adrenergic Receptors ◽  
Cyclase Activator ◽  
Adenylate Cyclase Activator ◽  
Muscarinic Agents

The K + current induced by isoprenaline acting on (β-adrenergic receptors in Xenopus laevis has been studied in oocytes still surrounded by their follicular cells and inner ovarian epithelium. Forskolin, an adenylate cyclase activator, induced a similar K + current and when used at subliminal concentration it potentiated the current induced by isoprenaline. Inhibition of phosphodiesterase by methylisobutylxanthine also en­hanced the response to isoprenaline. 8-Br-cAMP, a permeant analogue of cAMP also produced a K + current. Acetylcholine produced a long lasting inhibition of the isoprenaline current. This inhibition was not seen in the presence of atropine. It is concluded that the K + current induced by the activation of β-adrenergic receptors in the oocyte is mediated by an intracellular rise of cAMP.

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