Differential Changes in Lymphocyte β2-Adrenoceptor Density by β-Blocker Administration

Daul, A; Wang, Xiao L.; Borchard, U.; Bock, K. D.; Brodde, Otto‐Erich

doi:10.1097/00005344-198608004-00019

Cited by 22 publications

(10 citation statements)

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“…The pre sented data are the means of 16 experiments using MNC from different blood donors. Both the highdensity lymphocytes (HD; Percoll fraction 1) and the LD lymphocytes (Percoll fractions [7][8][9][10] were sensi tive to adrenaline-induced suppression of NKCC. The suppressing effect of adrenaline was dose-dependent at Final concentrations of 10-7-10_n M in both types of effector cells.…”

Section: Sensitivity O F Different Lymphocytementioning

confidence: 99%

“…Inhibition of NKCC can only be demonstrated if the cAMP-inducing agents are present during effector/target cell interaction. If the compounds are removed from NK effector lymphocytes by washing after a pretreatment period, NKCC may actually be enhanced, as shown for prostaglandin E2 [2] and vasointestinal peptide [5], Human lymphocytes bear (3-adrenergic receptors, which are target structures for the circulating cate cholamines adrenaline and noradrenaline [7,8], [3-Adrenergic receptors are coupled to adenylate cy clase, and the activation of these lymphocyte recep tors consequently induces the formation of intracellu lar cAMP [9,10], We have recently shown that adren aline effectively suppresses NKCC when added to mixtures of nonadherent lymphocytes and K 562 tar get cells. Pretreatment with adrenaline followed by removal of the drug resulted in the augmentation of NKCC.…”

Section: Introductionmentioning

confidence: 99%

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An Immunopharmacological Analysis of Adrenaline-Induced Suppression of Human Natural Killer Cell Cytotoxicity

Hellstrand

Hermodsson²

1989

Int Arch Allergy Immunol

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The circulating catecholamine adrenaline effectively suppressed human natural killer cell cytotoxicity (NKCC) when added to mixtures of effector lymphocytes and ⁵¹Cr-labelled target cells in a 4-hour ⁵¹Cr release assay in vitro. The effect was mimicked by the β₂-receptor agonist terbutaline but not by the β₁-receptor agonist prenalterol or the α₁/α₂-receptor agonist clonidine. Adrenaline-induced NKCC suppression was completely and potently antagonized by the mixed β₁/β₂-receptor antagonist propranolol and the selective β₂-receptor antagonist ICI 118,551 but not by the β₁-selective antagonist metoprolol. By comparing the adrenaline sensitivity of high-density (HD) and low-density (LD) lymphocytes, fractionated by Percoll density gradient centrifugation, we found that HD cells appeared more sensitive to adrenaline-induced suppression than LD cells. In both types of effector cells, adrenaline significantly suppressed NKCC at a final concentration of 10–11 M. Pretreatment of LD effector cells with IFN-α reduced the NKCC suppression by subsequent adrenaline treatment. Pretreatment with recombinant IL-2 virtually abolished the response to adrenaline. This effect was noted also when IL-2 and adrenaline were incubated simultaneously during the 4-hour ⁵¹Cr release assay. Our data suggest a role for adrenaline, via lymphocyte β²-receptor activation, in the regulation of natural killer cells.

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Section: Sensitivity O F Different Lymphocytementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

An Immunopharmacological Analysis of Adrenaline-Induced Suppression of Human Natural Killer Cell Cytotoxicity

Hellstrand

Hermodsson²

1989

Int Arch Allergy Immunol

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“…We have used standard therapeutic doses (with the exception of ICI 118,551, which is not available for therapeutic use) and have previously demonstrated that these doses are sufficient to up-regulate (propranolol, ICI 118,551 (Brodde etal., 1988;Daul etal., 1986)) or down-regulate lymphocyte 32-adrenoceptors (pindolol, (Daul et al, 1986)). The 13l-selective bisoprolol does not affect lymphocyte ,32-adrenoceptor number in therapeutic doses, but we have demonstrated that the dose used is sufficient to yield plasma levels which occupy > 85% of 13l-adrenoceptors Daul et al, 1986).…”

Section: Prostaglandin Elmentioning

confidence: 71%

Does treatment with beta‐adrenoceptor antagonists in vivo alter human adenylate cyclase responsiveness in vitro?

Michel

Klüppel

Philipp

et al. 1991

Brit J Clinical Pharma

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1. Treatment with beta‐adrenoceptor antagonists in vivo can alter adenylate cyclase responsiveness in the human heart. We have determined the effects of treatment with four different beta‐adrenoceptor antagonists in vivo on the responsiveness of lymphocyte and platelet adenylate cyclase in vitro in healthy volunteers. 2. Propranolol (non‐ selective, 4 x 40 mg day), bisoprolol (beta 1‐selective, 1 x 10 mg day), and ICI 118.551 (beta 2‐selective, 3 x 25 mg day) were tested as drugs without and pindolol (non‐selective, 2 x 5 mg day) as a drug with intrinsic sympathomimetic activity. Adenylate cyclase stimulation by GTP, prostaglandin E1 and forskolin was determined before, after a 7 day treatment period and 7 days after drug withdrawal. 3. Neither treatment with or withdrawal of any of the beta‐adrenoceptor antagonists altered adenylate cyclase responsiveness. 4. We conclude that adenylate cyclase responsiveness in circulating blood cells underlies different regulatory mechanisms than that in solid tissues such as the human heart. Our data suggest that circulating blood cells do not always reflect alterations in solid tissues.

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“…Celiprolol has been shown to possess partial agonist activity (ISA) at the beta adrenoreceptor in humans. Celiprolol reduced the density of beta 2 adrenoreceptors in human lymphocytes [34,35] and increased the sleeping heart rate in healthy volunteers in comparison to placebo [36], consistent with beta partial agonist activity.…”

Section: Discussionmentioning

confidence: 95%

Hemodynamic interactions of a new beta blocker, celiprolol, with nifedipine in angina pectoris

Silke¹,

Verma²,

1991

Cardiovasc Drug Ther

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The hemodynamic consequences of blockade at both beta-adrenoceptors and slow calcium channels is of therapeutic importance for patients with angina pectoris. The hemodynamic interaction of a new cardioselective beta blocker, celiprolol, and nifedipine was examined in an acute hemodynamic study using three prospectively matched groups with angiographically confirmed coronary artery disease (n = 10/group). Patients were randomly allocated to intravenous celiprolol (8 mg), sublingual nifedipine (20 mg), or their combination. Rest and exercise (supine bicycle) hemodynamics were determined before and following each therapy. At rest, celiprolol did not alter pumping function; nifedipine reduced diastolic blood pressure and systemic vascular resistance index (SVRI), with a small increase in heart rate. Combination therapy reduced systemic arterial pressure and SVRI; heart rate and cardiac stroke volume index increased. During exercise celiprolol tended to reduce heart rate and cardiac index; nifedipine reduced exercise SVR and cardiac stroke work indices. Combination therapy reduced all components of blood pressure; cardiac stroke work and SVR indices fell. These hemodynamic data suggest that beta blockade with celiprolol may result in a slight depression of cardiac pumping during exercise; however, such effects are offset by the vasodilating actions of nifedipine (reflex sympathetic action offsetting cardiodepression). Thus the acute hemodynamic effects of this combination were seemingly safe in these patients; the longer term effects during maintained therapy should be further assessed.

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Differential Changes in Lymphocyte β2-Adrenoceptor Density by β-Blocker Administration

Cited by 22 publications

References 0 publications

An Immunopharmacological Analysis of Adrenaline-Induced Suppression of Human Natural Killer Cell Cytotoxicity

An Immunopharmacological Analysis of Adrenaline-Induced Suppression of Human Natural Killer Cell Cytotoxicity

Does treatment with beta‐adrenoceptor antagonists in vivo alter human adenylate cyclase responsiveness in vitro?

Hemodynamic interactions of a new beta blocker, celiprolol, with nifedipine in angina pectoris

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