Influence of sex‐steroid hormones on the regulation of lymphocyte beta 2‐adrenoceptors during the menstrual cycle.

Wheeldon, NM; Newnham, D M; Coutie, Wendy J.; Peters, JA; McDevitt, DG; Lipworth, BJ

doi:10.1111/j.1365-2125.1994.tb04308.x

Cited by 74 publications

(47 citation statements)

References 19 publications

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“…Indeed, some studies reported that the luteal phase is characterized by higher expression of β 2 -adrenoceptors on lymphocytes, and by a higher lymphocyte cAMP response to isoproterenol (Wheeldon et al, 1994). While NK cells comprise only about 15% of the lymphocyte population, they were reported to express the highest levels of β 2 -adrenoceptors (Landmann, 1992).…”

Section: Discussionmentioning

confidence: 99%

Timing within the menstrual cycle, sex, and the use of oral contraceptives determine adrenergic suppression of NK cell activity

Shakhar

Rosenne

et al. 2000

Br J Cancer

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Physiological responses that involve adrenergic mechanisms, such as stress-induced changes in cardiovascular indices, were reported to fluctuate along the menstrual cycle. Metastatic development following surgery was also reported to vary according to the menstrual phase during which a primary breast tumour was removed. Natural killer (NK) cells are believed to play an important role in controlling metastases. Our recent studies in rats demonstrated that adrenergic suppression of NK activity and of resistance to metastasis is more profound during oestrous phases characterized by high levels of oestradiol. In the current study in humans, we examined the in vitro impact of a β-adrenergic agonist, metaproterenol (MP), on NK activity, comparing blood drawn from (a) women tested at 3–4 different phases of their menstrual cycle ( n = 10), (b) women using oral contraceptives (OC) ( n = 10), and (c) men ( n = 7). NK activity in each blood sample was assessed in the presence of 5 different concentrations of MP (10 –8 M to 10 –6 M), and in its absence (baseline). The results indicated marked group differences in the magnitude of NK suppression by MP: EC 50 was 2.6-fold lower in the luteal phase compared to the follicular phase, and 1.8-fold lower in OC users compared to men, who were least susceptible to the effects of MP. No significant group differences or menstrual effects in baseline levels of NK activity were evident. These findings provide the first empirical evidence for menstrual regulation of adrenergic impact on cellular immune competence. Relevance of these findings to the relation between the timing of breast cancer excision within the menstrual cycle and survival rates is discussed. © 2000 Cancer Research Campaign http://www.bjcancer.com

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Section: Discussionmentioning

confidence: 99%

Timing within the menstrual cycle, sex, and the use of oral contraceptives determine adrenergic suppression of NK cell activity

Shakhar

Rosenne

et al. 2000

Br J Cancer

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“…Previous reports in this area have not been consistent in terms of gender difference. Wheeldon et al (1994) reported that females showed higher lymphocyte ␤ 2 -adrenoceptor density (B max ) and stimulated cAMP levels only during luteal phase than male subjects. Halper et al (1984) reported that betareceptor binding indices (B max ) in general did not differ between males and females; whereas, in older subjects, females showed higher cAMP ratio levels than males.…”

Section: Discussionmentioning

confidence: 99%

Psychological States and Lymphocyte β-Adrenergic Receptor Responsiveness

Dimsdale

Mills

1999

Neuropsychopharmacology

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There is a complex interplay between psychological states and biochemical factors. ␤ -Adrenergic receptor responsiveness is altered in some patients with depression and anxiety disorders, but the relation between various psychological states and receptor function in a normal population is unknown. We measured lymphocyte ␤ -adrenergic receptor density (B max ), sensitivity (cAMP ratio), the Profile of Mood States (POMS), and Spielberger State-TraitThere is a strong interplay between psychological states and physiology. This interplay has traditionally been studied extensively in terms of hormonal levels. More recently, investigators have begun to explain how such factors relate to receptor physiology. ␤ -Adrenergic receptor responsiveness may be altered in patients with such psychiatric diseases as depression (Pandey et al. 1987;Magliozzi et al. 1989) and panic disorder (Nesse et al. 1984;Brown et al. 1988;Aronson et al. 1989). In panic disorder, reduced ␤ -adrenergic receptor responsiveness has been noted in two ways, with both reduced receptor density and reduced responsivity to isoproterenol (Maddock et al. 1993).Adrenergic receptor regulation is closely related to psychological stressors (Graafsma et al. 1989). ␤ -Adrenergic receptor function is closely affected by numerous psychological stressors; for example, individuals with high life stress have lower ␤ -adrenergic receptor sensitivity (Dimsdale et al. 1994). Recently, hostility has been shown to be associated with ␤ -adrenergic receptor down-regulation in healthy young males (Suarez et al. 1997). All of these studies suggest that adrenergic receptors may be regarded as an important link between humoral signals influenced by psychological stressors and end organ responsiveness. However, normative information still needs to be acquired concerning the relationship between various psychological states and ␤ -adrenergic receptor responsiveness in a nonpsychiatric population.Human leukocytes offer a useful model for studying the role of ␤ -adrenergic receptor responsiveness in patients with medical or psychiatric illness (Pandey et al. . The use of lymphocyte ␤ -adrenergic receptors as a model for central ␤ -receptors is not as well established as the use of lymphocyte ␤ -receptors for such peripheral tissues as the heart and lung. Nonetheless, Mann et al. (1990) reported a normalization of blunted lymphocyte ␤ -receptors in depression following treatment. In addition, Brodde et al. (1986) reported that alterations in lymphocyte ␤ -adrenoceptors mirror changes in ␤ -adrenoceptors in other tissues less accessible in human studies. There are two major techniques for measuring ␤ -adrenergic receptor responsiveness in human leukocytes; measuring receptor density (B max ) and sensitivity. ␤ -Adrenergic receptor density in lymphocytes is defined as the number of receptors/cell for intact cells, and as pico-or femto-moles/mg protein for membranes. ␤ -Adrenergic receptor sensitivity is defined as the efficiency with which agonist binding translates into stimulation...

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“…Since β 2 -adrenergic mechanisms have been reported to be sexually dimorphic (Barker et al, 2005;de Coupade et al, 2004;Hinojosa-Laborde et al, 1999;Krieg et al, 1986;Mills et al, 1996;Tan et al, 1997;Wheeldon et al, 1994), the present study investigated the ability of β 2 -adrenergic receptors to modulate neutrophil recruitment, using wild-type (FVB) and β 2 -adrenergic receptor knockout mice (bred on a congenic FVB background). Of note, in a comparison of inflammation in the lungs of 9 mouse strains, after ovalbumin sensitization and aerosol challenge the FVB strain had fewer infiltrating leukocytes than 4 other strains, but similar to BALB/C, C57/BL and C3H/HeJ strains (Whitehead et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

β2-Adrenergic receptor-dependent sexual dimorphism for murine leukocyte migration

Coupade¹,

Brown²,

Dazin

et al. 2007

Journal of Neuroimmunology

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In wild-type FVB mice, leukocyte recruitment to lipopolysaccharide was sexually dimorphic, with a greater number of leukocytes recruited in females. In male β 2 -adrenergic receptor knock out mice (bred on a congenic FVB background) the number leukocytes recruited was increased ~4-fold, while in females there was no change, eliminating sexual dimorphism in leukocyte migration. While there were significantly fewer recruited CD62L + and CD11a + leukocytes in wild-type males, only in male β 2 -adrenergic receptor knock out mice was there an increase in the number of recruited CD11a + leukocytes, again eliminating sexual dimorphism. Thus, leukocyte migration and CD11a + adhesion molecule expression in male, but not in female, leukocytes is β 2 -adrenergic receptor-dependent. Our findings provide support for a role of β 2 -adrenergic receptor mechanisms in the inflammatory response, and suggest that β 2 -adrenergic receptor on male leukocytes contributes to sexual dimorphism in the effect of stress on inflammatory diseases.

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Influence of sex‐steroid hormones on the regulation of lymphocyte beta 2‐adrenoceptors during the menstrual cycle.

Cited by 74 publications

References 19 publications

Timing within the menstrual cycle, sex, and the use of oral contraceptives determine adrenergic suppression of NK cell activity

Timing within the menstrual cycle, sex, and the use of oral contraceptives determine adrenergic suppression of NK cell activity

Psychological States and Lymphocyte β-Adrenergic Receptor Responsiveness

β2-Adrenergic receptor-dependent sexual dimorphism for murine leukocyte migration

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