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

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 beta-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 I-II. 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 beta-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 beta-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.

[1]  H. Motulsky,et al.  A new method for isolation of human lymphocyte subsets reveals differential regulation of β‐adrenergic receptors by terbutaline treatment , 1989, Clinical pharmacology and therapeutics.

[2]  M. Packer,et al.  Neurohormonal interactions and adaptations in congestive heart failure. , 1988, Circulation.

[3]  J. Cohn,et al.  Prognosis of congestive heart failure and predictors of mortality. , 1988, The American journal of cardiology.

[4]  G. Kammer The adenylate cyclase-cAMP-protein kinase A pathway and regulation of the immune response. , 1988, Immunology today.

[5]  K. Madden,et al.  Noradrenergic Sympathetic Neural Interactions with the Immune System: Structure and Function , 1987, Immunological reviews.

[6]  G. Hunninghake,et al.  Beta-adrenergic-receptor-mediated suppression of interleukin 2 receptors in human lymphocytes. , 1987, Journal of immunology.

[7]  M. Michel,et al.  Arterial hypotension in chronic hemodialyzed patients. , 1987, Kidney international.

[8]  H. Motulsky,et al.  Receptor redistribution does not accompany terbutaline‐induced down regulation of beta‐adrenergic receptors on human mononuclear leukocytes , 1987, Clinical pharmacology and therapeutics.

[9]  H. Motulsky,et al.  In vivo regulation of beta-adrenergic receptors on human mononuclear leukocytes: assessment of receptor number, location, and function after posture change, exercise, and isoproterenol infusion. , 1986, The Journal of clinical endocrinology and metabolism.

[10]  L. Lanier,et al.  Lectin-dependent and anti-CD3 induced cytotoxicity are preferentially mediated by peripheral blood cytotoxic T lymphocytes expressing Leu-7 antigen. , 1986, Journal of immunology.

[11]  P. Erne,et al.  Changes of immunoregulatory cells induced by psychological and physical stress: relationship to plasma catecholamines. , 1984, Clinical and experimental immunology.

[12]  N. Miller,et al.  Stress-induced suppression of immunity in adrenalectomized rats. , 1983, Science.

[13]  H. Weiner,et al.  Epinephrine-induced changes in the distribution of lymphocyte subsets in peripheral blood of humans. , 1983, Journal of immunology.

[14]  S M Ryan,et al.  Coping and immunosuppression: inescapable but not escapable shock suppresses lymphocyte proliferation. , 1983, Science.

[15]  J. Carlquist,et al.  DEFICIENT NATURAL KILLER CELL ACTIVITY IN PATIENTS WITH IDIOPATHIC DILATED CARDIOMYOPATHY , 1982, The Lancet.

[16]  R. Eckstein,et al.  Reduced Suppressor Cell Activity in Congestive Cardiomyopathy and in Myocarditis , 1982, Circulation.

[17]  Weber Ma,et al.  The sympathetic nervous system in primary hypertension. , 1982 .

[18]  J. Drayer,et al.  The sympathetic nervous system in primary hypertension. , 1982, Mineral and electrolyte metabolism.

[19]  D. O'Connor,et al.  Adrenergic receptors in human and experimental pheochromocytoma. , 1982, Clinical and experimental hypertension. Part A, Theory and practice.

[20]  D. Hoyer,et al.  The β-adrenergic receptor in human lymphocytes: Subclassification by the use of a new radio-ligand, (±)−125iodocyanopindolol , 1981 .

[21]  N. Miller,et al.  Suppression of immunity by stress: effect of a graded series of stressors on lymphocyte stimulation in the rat. , 1981, Science.

[22]  M. Ziegler,et al.  A sensitive radioenzymatic assay for catechol drugs , 1980, Journal of neuroscience research.

[23]  M. Collector,et al.  Stress-induced modulation of the immune response. , 1977, Science.

[24]  G. Ahlborg,et al.  Exercise leukocytosis with and without beta-adrenergic blockade. , 2009, Acta medica Scandinavica.

[25]  A. M. Lands,et al.  Differentiation of Receptor Systems activated by Sympathomimetic Amines , 1967, Nature.