The β-adrenergic receptor in human lymphocytes: Subclassification by the use of a new radio-ligand, (±)−125iodocyanopindolol

Brodde, Otto‐Erich; Engel, G.; Hoyer, Daniel; Bock, K. D.; Weber, Florence

doi:10.1016/0024-3205(81)90490-2

Cited by 206 publications

(50 citation statements)

References 9 publications

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“…Despite an acceptably low level of non-specific (non-displaceable by (-)-isoprenaline) binding of the order of 15-30% of total binding, saturation binding assays gave unacceptably erratic Scatchard plots. In radioligand association binding studies we observed that equilibrium binding was not attained within 60min, in agreement with others (Brodde et al, 1981;Engel et al, 1981). The large cyano grouping on the radioligand molecule may impede its access to the binding site of the P-adrenoceptor, thus increasing the time to reach equilibrium (cf.…”

Section: Methodssupporting

confidence: 69%

Characterization of rat liver β‐adrenoceptors during perinatal development as determined by [¹²⁵I]‐iodopindolol radioligand binding assays

Snell

Evans

1988

British J Pharmacology

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Section: Methodssupporting

confidence: 69%

Characterization of rat liver β‐adrenoceptors during perinatal development as determined by [¹²⁵I]‐iodopindolol radioligand binding assays

Snell

Evans

1988

British J Pharmacology

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“…The spleen and other lymphoid tissues are densely innervated with sympathetic nerve fibers (5), and lymphocytes have #2-adrenergic receptors that couple to stimulation of adenylate cyclase (10). Numerous in vitro studies have shown that treatment of human lymphocytes with the f3-adrenergic agonist isoproterenol (and other agents that elevate intracellular cAMP concentrations) reduces mitogen-induced increases in intracellular inositol-(1,4,5)-trisphosphate and calcium, production of IL-2 and IFN, expression of IL-2 receptors, immune cytolysis, antibody production, and plaque formation on sheep red blood cells, as well as IL-1 production by monocytes (for review, 1 1-13).…”

Section: Discussionmentioning

confidence: 99%

Adrenergic control of circulating lymphocyte subpopulations. Effects of congestive heart failure, dynamic exercise, and terbutaline treatment.

Maisel¹,

Knowlton²,

Fowler³

et al. 1990

J. Clin. Invest.

136

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The current studies were undertaken to explore the relationship between enhanced sympathetic nervous activity and lymphocyte subset distribution in three settings: congestive heart failure, dynamic exercise, and fl-adrenergic agonist treatment.We compared the number and subset distribution of circulating lymphocytes in 36 patients with congestive heart failure and 31 age-matched control subjects. The number of circulating lymphocytes was lower in heart failure than in control. This was due to a reduction in Tsuppressor/cytotoxic and natural killer cells without significant alteration of Thelper cells. The extent of the alteration was similar in patients with idiopathic and ischemic heart failure, but the reduction was more pronounced in patients with New York Heart Association class III-IV than in class 1-11. The plasma catecholamine elevation in heart failure was also independent of etiology but more pronounced in the more severely ill patients. We also assessed lymphocyte subsets after acute stimulation of sympathetic activity by dynamic exercise and after treatment with the ,8-adrenergic agonist terbutaline. Dynamic exercise until exhaustion increased the number of circulating lymphocytes in healthy controls and heart failure patients in a subset-selective manner. By contrast, a 7-d treatment with terbutaline caused a reduction in the circulating number of lymphocytes in some subsets that was identical to that seen in heart failure patients. We conclude that prolonged sympathetic activity reduces the number of circulating lymphocytes by a fi-adrenergic mechanism. Such alterations might be involved in the pathophysiology of heart failure and other disease states involving increased activity of the sympathetic nervous system. (J. Clin. Invest. 1990. 85:462-467.) beta receptors -lymphocytes -heart failuresympathetic nervous system

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“…The restoration of an agonist-promoted downregulation of the ß-adrenoceptors by glucocorticoids has also been reported in human and equine mononuclear leukocytes (neutrophils and lymphocytes) [6][7][8]. It is generally supposed that these cells contain a homogeneous population of the ß 2 -subtype [9], which couples via G s protein to the adenylyl cyclase system, and reflect drugand disease-induced changes in other solid tissues, e.g., heart and myometrium [10,11]. However, it is not known whether the lymphocyte ß 2 -adrenergic receptors (ß 2 AR) can be enhanced by prolonged intravenously administered short-acting dexamethasone.…”

Section: Introductionmentioning

confidence: 99%

Dexamethasone-Induced Increase in Lymphocyte β-Adrenergic Receptor Density and cAMP Formation in vivo

Abraham

Schusser²,

Ungemach³

2002

Pharmacology

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The influence of dexamethasone on the density of β₂-adrenergic receptors (β₂-adrenergic receptors (β₂AR) and on the intracellular adenosine 3′,5′-cyclic monophosphate (cAMP) response was studied in equine lymphocytes in vivo. Dexamethasone (0.1 mg/kg/day, 1–5 days) raised the number of β₂AR – B_max as assessed by (–)-[¹²⁵I]iodocyanopindolol binding (ICYP) – to 2.5- to 3.5-fold as compared with control values. The increase in β₂AR number was fast (342 ± 49 vs. 960 ± 103 binding sites/lymphocyte after 24 h), reaching a maximum between 48 and 96 h (342 ± 49 vs. 1,289 ± 150 and 1,106 ± 68 binding sites/lymphocyte, respectively). The isoprenaline-induced cAMP accumulation (measured by a [³H]-cAMP radioimmunoassay system) was concomitantly enhanced by dexamethasone (1.5- to 2.4-fold). Both parameters were reversible to a similar rate at dexamethasone withdrawal. The changes in the functional responsiveness of lymphocytes were not reflected by changes in the binding affinity for ICYP of β₂AR. These results demonstrate the in vivo glucocorticoid-mediated regulation of β₂AR in equine lymphocytes which has already been suggested on the basis of in vitro observations in other tissues.

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The β-adrenergic receptor in human lymphocytes: Subclassification by the use of a new radio-ligand, (±)−125iodocyanopindolol

Cited by 206 publications

References 9 publications

Characterization of rat liver β‐adrenoceptors during perinatal development as determined by [¹²⁵I]‐iodopindolol radioligand binding assays

Characterization of rat liver β‐adrenoceptors during perinatal development as determined by [¹²⁵I]‐iodopindolol radioligand binding assays

Adrenergic control of circulating lymphocyte subpopulations. Effects of congestive heart failure, dynamic exercise, and terbutaline treatment.

Dexamethasone-Induced Increase in Lymphocyte β-Adrenergic Receptor Density and cAMP Formation in vivo

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The β-adrenergic receptor in human lymphocytes: Subclassification by the use of a new radio-ligand, (±)−125iodocyanopindolol

Cited by 206 publications

References 9 publications

Characterization of rat liver β‐adrenoceptors during perinatal development as determined by [125I]‐iodopindolol radioligand binding assays

Characterization of rat liver β‐adrenoceptors during perinatal development as determined by [125I]‐iodopindolol radioligand binding assays

Adrenergic control of circulating lymphocyte subpopulations. Effects of congestive heart failure, dynamic exercise, and terbutaline treatment.

Dexamethasone-Induced Increase in Lymphocyte β-Adrenergic Receptor Density and cAMP Formation in vivo

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Characterization of rat liver β‐adrenoceptors during perinatal development as determined by [¹²⁵I]‐iodopindolol radioligand binding assays

Characterization of rat liver β‐adrenoceptors during perinatal development as determined by [¹²⁵I]‐iodopindolol radioligand binding assays