Uterine β-adrenergic receptors in allogeneic and syngeneic pregnancy

1994 ◽  
Vol 72 (5) ◽  
pp. 456-462 ◽  
Author(s):  
Maria Elena Sales ◽  
Enri S. Borda
Keyword(s):  
Cyclic Amp ◽  
Binding Sites ◽  
Adrenergic Receptors ◽  
Binding Assay ◽  
Binding Assays ◽  
Receptor Affinity ◽  
Number Of Binding Sites ◽  
Β Receptor ◽  
Β Adrenergic Receptors

Two different mechanisms of regulation in uterine β-adrenergic receptors in allogeneic pregnancy (AP) and syngeneic pregnancy (SP) are described in this work. Firstly we noted changes in β-adrenergic sensitivity to isoproterenol in AP, while in SP differences in uterine reactivity to isoproterenol were found. In binding assays with the β-antagonist [3H]dihydroalprenolol, changes in β-receptor affinity were seen in AP, while in SP the maximal number of binding sites is altered. In addition, there are differences in uterine concentrations of cyclic AMP in both types of pregnancies as well as in the nucleotide response to isoproterenol. The differences in the reactivity and expression of uterine β-adrenoceptors in both types of pregnancies may be due to a distinctive immunological role of the semiallogeneic fetus in AP.Key words: β-adrenoceptors, cyclic AMP production, uterus, contractility, binding assay, syngeneic pregnancy, allogeneic pregnancy.

β-Adrenergic regulation of Na+ uptake by larval zebrafish Danio rerio in acidic and ion-poor environments

2012 ◽  
Vol 303 (10) ◽  
pp. R1031-R1041 ◽  
Author(s):  
Yusuke Kumai ◽  
Mellissa A. R. Ward ◽  
Steve F. Perry
Keyword(s):  
Danio Rerio ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Receptor Agonist ◽  
Acidic Water ◽  
Adrenergic Systems ◽  
Β Receptor ◽  
Β Adrenergic Receptors ◽  
Adrenergic Receptor Agonist

The potential role of adrenergic systems in regulating Na+ uptake in zebrafish ( Danio rerio) larvae was investigated. Treatment with isoproterenol (a generic β-adrenergic receptor agonist) stimulated Na+ uptake, whereas treatment with phenylephrine (an α1-adrenergic receptor agonist) as well as clonidine (an α2-adrenergic receptor agonist) significantly reduced Na+ uptake, suggesting opposing roles of α- and β-adrenergic receptors in Na+ uptake regulation. The increase in Na+ uptake associated with exposure to acidic water (pH = 4.0) was attenuated in the presence of the nonselective β-receptor antagonist propranolol or the β1-receptor blocker atenolol; the β2-receptor antagonist ICI-118551 was without effect. The stimulation of Na+ uptake associated with ion-poor water (32-fold dilution of Ottawa tapwater) was unaffected by β-receptor blockade. Translational gene knockdown of β-receptors using antisense oligonucleotide morpholinos was used as a second method to assess the role of adrenergic systems in the regulation of Na+ uptake. Whereas β1- or β2B-receptor knockdown led to significant decreases in Na+ uptake during exposure to acidic water, only β2A-receptor morphants failed to increase Na+ uptake in response to ion-poor water. In support of the pharmacology and knockdown experiments that demonstrated an involvement of β-adrenergic systems in the control of Na+ uptake, we showed that the H+-ATPase-rich (HR) cell, a subtype of ionocyte known to be a site of Na+ uptake, is innervated and appears to express β-adrenergic receptors (propranolol binding sites) at 4 days postfertilization. These data indicate an important role of adrenergic systems in regulating Na+ uptake in developing zebrafish.

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.

Decreased glucagon binding and glucagon-stimulated lipolysis in adipocytes from streptozotocin-diabetic rats

1989 ◽  
Vol 121 (5) ◽  
pp. 705-713 ◽  
Author(s):  
Nobuyuki Sato ◽  
Minoru Irie ◽  
Hiroshi Kajinuma ◽  
Kazuo Suzuki
Keyword(s):  
Quantitative Analysis ◽  
Cyclic Amp ◽  
Adrenergic Receptors ◽  
Marked Reduction ◽  
Diabetic Rats ◽  
Down Regulation ◽  
Streptozotocin Diabetic Rats ◽  
Β Adrenergic Receptors ◽  
Glucagon Receptors ◽  
The Relationship

Abstract. Adipocytes from streptozotocin-diabetic rats showed a markedly reduced lipolytic response to glucagon concomitant with a 90% or greater decrease in the number of glucagon receptors per cell. In contrast, β-adrenergic receptors assessed by [3H]dihydroalprenolol binding and lipolysis stimulated by isoproterenol, dibutyryl 3′5′-cyclic AMP and 3-isobutyl-1-methylxanthine were reduced by only 10–25% in diabetic rats compared with controls. Furthermore, quantitative analysis of the relationship between the amount of cell-bound glucagon and the hormone-stimulated lipolysis revealed that the function of the remaining 10% of glucagon receptors remained intact in cells from diabetic animals. These findings suggest that the lipolytic cascades, including β-adrenergic receptors, in adipocytes are not greatly impaired by diabetes, and therefore, the unresponsiveness of these cells to glucagon is mostly due to a marked reduction in the number of glucagon receptors, probably as a result of a down-regulation by postprandial hyperglucagonemia.

scholarly journals Thyroid-hormone modulation of the number of β-adrenergic receptors in rat fat-cell membranes

1978 ◽  
Vol 176 (3) ◽  
pp. 1007-1010 ◽  
Author(s):  
Y Giudicelli
Keyword(s):  
Thyroid Hormone ◽  
Binding Sites ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Receptor Density ◽  
Beta Adrenergic Receptors ◽  
Fat Cell ◽  
Beta Adrenergic ◽  
Hormone Modulation ◽  
Β Adrenergic Receptors

Adipocytes from thyroidectomized rats contain 3 times less [3H]dihydroalprenolol-binding sites (beta-adrenergic receptors) than adipocytes from euthyroid animals. This alteration is not solely due to cell-size differences, but also to a thyroidectomy-induced defect in beta-adrenergic receptor density per adipocyte surface area, a defect that is furthermore corrected by tri-iodothyronine treatment.

Endothelin ETA and ETB receptors in postnatal intestine

2001 ◽  
Vol 280 (4) ◽  
pp. G555-G562 ◽  
Author(s):  
Craig A. Nankervis ◽  
David J. Dunaway ◽  
Charles E. Miller
Keyword(s):  
Binding Sites ◽  
Specific Binding ◽  
Ischemia Reperfusion ◽  
Age Groups ◽  
Scatchard Analysis ◽  
Binding Assays ◽  
Site Model ◽  
Number Of Binding Sites ◽  
Competitive Binding Assays

We aimed to characterize endothelin (ET) receptors in the swine intestinal vasculature and to determine ischemia-reperfusion (I/R) effects on these receptors. Saturation and competitive binding assays were performed on mesenteric artery protein membranes from 1- and 40-day-old animals, both control and those subjected to 1 h of partial ischemia followed by 6 h of reperfusion in vivo. Scatchard analysis of saturation binding with 125I-labeled ET-1 in membranes from endothelium-denuded (E−) vessels revealed that the maximum number of binding sites was greater in younger animals. Competitive125I-ET-1 binding was significant for a one-site model with ET-1, ET-3, and sarafotoxin S6c (S6c) in membranes from endothelium-intact (E+) and E− vessels in both age groups. The maximum number of ET-1 binding sites was significantly greater in younger animals. In the presence of the ETAreceptor antagonist BQ-123, competitive 125I-ET-1 binding was significant for a one-site model with ET-1 and S6c in membranes from E+ vessels in both age groups. The maximum number of ET-1 binding sites was significantly greater in younger animals. After I/R, the maximum number of ET-1 binding sites was unchanged. In the presence of BQ-123, specific binding by ET-1 and S6c was eliminated in both age groups after I/R. These results suggest that both ET receptor populations are expressed to a greater degree in younger animals and I/R significantly affects the ETB receptor.

Adrenergic receptors on cerebral microvessels: pericyte contribution

1989 ◽  
Vol 256 (1) ◽  
pp. R224-R230 ◽  
Author(s):  
R. M. Elfont ◽  
P. R. Sundaresan ◽  
C. D. Sladek
Keyword(s):  
Endothelial Cells ◽  
Binding Sites ◽  
Adrenergic Receptors ◽  
Radioligand Binding ◽  
Dissociation Constants ◽  
Specific Binding ◽  
Binding Studies ◽  
Cerebral Microvessels ◽  
Beta Adrenoceptor ◽  
Number Of Binding Sites

R224-R230, 1989.--[125I]iodocyanopindolol ([125I]ICYP) and [3H]rauwolscine were used to quantitate, respectively, the beta- and alpha 2-adrenergic receptors in freshly isolated bovine cerebral microvessels and in pericyte cultures derived from these microvessels. Morphological and immunocytochemical criteria distinguished the pericytes from endothelial cells. Competitive binding studies established the specificity of the radioligand binding. The maximal number of binding sites (Bmax) for [125I]ICYP in the pericytes constituted only 8% of that in the microvessels (3.5 +/- 1.3 vs. 44.4 +/- 6.6 fmol/mg protein). In contrast, the Bmax for [3H]rauwolscine in the pericytes was 50% of that in the microvessels (55.4 +/- 11.8 vs. 111.1 +/- 9.5 fmol/mg protein). The dissociation constants for both [125I]ICYP and [3H]rauwolscine were similar in the two preparations. No alpha 1-adrenergic receptors, as defined by the specific binding of [3H]prazosin, were identified either in the pericytes or microvessels. Overall, our results suggest that pericytes contribute minimally to the total beta-adrenoceptor number of cerebral microvessels, and thus the beta-adrenoceptors must be located predominantly on endothelial cells. However, the contribution of pericytes to the total alpha 2-adrenoceptor number of the microvessels may be substantial.

Modification of cardiac adrenergic receptors by oxygen free radicals

1991 ◽  
Vol 260 (3) ◽  
pp. H821-H826 ◽  
Author(s):  
M. Kaneko ◽  
D. C. Chapman ◽  
P. K. Ganguly ◽  
R. E. Beamish ◽  
N. S. Dhalla
Keyword(s):  
Free Radicals ◽  
Xanthine Oxidase ◽  
Binding Sites ◽  
Adrenergic Receptors ◽  
Oxygen Free Radicals ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Alpha Adrenergic Receptors ◽  
Cgp 12177 ◽  
Number Of Binding Sites

To examine the effects of oxygen free radicals on alpha- and beta-adrenergic receptors, rat heart crude membranes were incubated with xanthine plus xanthine oxidase, H2O2, or H2O2 plus Fe2+. The assay of beta-adrenergic receptors involving [3H]dihydroalprenolol (DHA) binding revealed that the maximal number of binding sites (Bmax) and dissociation constant (Kd) were increased by xanthine plus xanthine oxidase. H2O2 increased the Kd value for [3H]DHA binding. When a hydrophilic ligand, [3H]CGP-12177, was used for the beta-adrenergic receptor assay, an increase in Kd value without any changes in Bmax value was evident on treating the membranes with xanthine plus xanthine oxidase. The assay of alpha-adrenergic receptors involving [3H]prazosin binding showed a decrease in the number of binding sites and an increase in Kd value only after a prolonged period of incubation. Both H2O2 and H2O2 plus Fe2+ increased the Kd value for [3H]prazosin without changes in Bmax. Changes in both alpha- and beta-adrenergic receptors similar to those with crude membranes were also seen by employing the purified heart sarcolemmal membranes. These data indicate that adrenergic receptors in the sarcolemmal membranes are modified by oxygen free radicals.

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.

α-Adrenergic receptors modulate β-receptor affinity in rat kidney membranes

Nature ◽  
1980 ◽  
Vol 286 (5769) ◽  
pp. 159-160 ◽  
Author(s):  
Elizabeth A. Woodcock ◽  
Colin I. Johnston
Keyword(s):  
Adrenergic Receptors ◽  
Rat Kidney ◽  
Receptor Affinity ◽  
Β Receptor
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