Adrenergic Function in Patients With Panic Anxiety

Nesse, Randolph M.; Cameron, Oliver G.; Curtis, George C.; McCann, Daisy S.; Huber-Smith, Marla J.

doi:10.1001/archpsyc.1984.01790190045005

Cited by 250 publications

(80 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…It is known that the physiology of peripheral lymphocyte ␤-adrenergic receptors may be altered in patients with anxiety disorders, especially for panic disorder. Nesse et al (1984) suggested that ␤-adrenergic receptors are down-regulated in patients with panic disorder. Most studies regarding ␤-adrenergic receptor binding and adrenergically mediated lymphocyte cAMP production also show a reduction in panic disorder (Maddock et al 1993;Abelson and Cameron 1994).…”

Section: Discussionmentioning

confidence: 99%

“…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).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Psychological States and Lymphocyte β-Adrenergic Receptor Responsiveness

Dimsdale

Mills

1999

Neuropsychopharmacology

View full text Add to dashboard Cite

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...

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Psychological States and Lymphocyte β-Adrenergic Receptor Responsiveness

Dimsdale

Mills

1999

Neuropsychopharmacology

View full text Add to dashboard Cite

show abstract

“…Panic disorder patients have higher baseline HR than controls (Gorman et al, 1983;Nesse et al, 1984) and electrocardiograms in panic disorder patients reveal sympathetic dominance and parasympathetic withdrawal (Hamada et al, 1998;McCraty et al, 2001). Panic disorder patients also show disrupted baroreceptor function that persists even when they are in remission (Shioiri et al, 2005).…”

Section: Pathways For Lactate-induced Panic-like Responsesmentioning

confidence: 99%

Neural Pathways Underlying Lactate-Induced Panic

Johnson

Truitt

Fitz

et al. 2007

Neuropsychopharmacol

View full text Add to dashboard Cite

Panic disorder is a severe anxiety disorder characterized by susceptibility to induction of panic attacks by subthreshold interoceptive stimuli such as 0.5 M sodium lactate infusions. Although studied for four decades, the mechanism of lactate sensitivity in panic disorder has not been understood. The dorsomedial hypothalamus/perifornical region (DMH/PeF) coordinates rapid mobilization of behavioral, autonomic, respiratory and endocrine responses to stress, and rats with disrupted GABA inhibition in the DMH/PeF exhibit panic-like responses to lactate, similar to panic disorder patients. Utilizing a variety of anatomical and pharmacological methods, we provide evidence that lactate, via osmosensitive periventricular pathways, activates neurons in the compromised DMH/PeF, which relays this signal to forebrain limbic structures such as the bed nucleus of the stria terminalis to mediate anxiety responses, and specific brainstem sympathetic and parasympathetic pathways to mediate the respiratory and cardiovascular components of the panic-like response. Acutely restoring local GABAergic tone in the DMH/PeF blocked lactate-induced panic-like responses. Autonomic panic-like responses appear to be a result of DMH/PeF-mediated mobilization of sympathetic responses (verified with atenolol) and resetting of the parasympathetically mediated baroreflex. Based on our findings, DMH/PeF efferent targets such as the C1 adrenergic neurons, paraventricular hypothalamus, and the central amygdala are implicated in sympathetic mobilization; the nucleus of the solitary tract is implicated in baroreflex resetting; and the parabrachial nucleus is implicated in respiratory responses. These results elucidate neural circuits underlying lactate-induced panic-like responses and the involvement of both sympathetic and parasympathetic systems.

show abstract

“…In fact, there is some evidence that the hypothalamic pituitary-adrenal (HPA) system is overactive in patients with PD, but up to now the data have been inconclusive. Baseline plasma levels of cortisol were reported to be elevated in panic patients by some authors (Goldstein et al 1987;Nesse et al 1984;Roy-Byrne et al 1986). (Hollander et al 1989) found elevated baseline plasma cortisol levels only in a subgroup of panic patients.…”

Section: The Hypothalamic-pituitary-adrenal System In Pdmentioning

confidence: 96%

Smoking Modulates Neuroendocrine Responses to Ipsapirone in Patients with Panic Disorder

Broocks

Bandelow

Koch

et al. 2002

Neuropsychopharmacology

View full text Add to dashboard Cite

Reduced 5-HT1A-receptor responsiveness has been reported in patients with panic disorder(PD) and/or agoraphobia (PDA). Although many of these patients are regular smokers, it has not been examined whether psychological or neurobiological effects induced by the selective 5-HT1A-receptor agonist, ipsapirone, are affected by the smoking status of the patients.In order to clarify this question neuroendocrine challenges with oral doses of ipsapirone (0.3 mg/kg) Neuropharmacological challenges with the selective 5-hydroxytryptamine-1A (5-HT1A) receptor agonist, ipsapirone, have been used in several studies to assess 5-HT1A-receptor related functions in patients suffering from various neuropsychiatric disorders (Broocks et al. 2000;Lesch et al. 1990a;Lesch et al. 1991;Lesch et al. 1990b;Lesch et al. 1992) and in healthy controls (Broocks et al. 1999;Kahn et al. 1994;Lesch et al. 1990c;Lesch et al. 1990d).Indices of abnormal serotonergic function have been reported in patients with panic disorder (PD) and/or agoraphobia (PDA). In particular, there is evidence for an increased sensitivity of the 5-HT 2C subsystem (Charney et al. 1987a;Charney et al. 1987b;Kahn et al. 1988a Kahn and Wetzler 1991;Kahn et al. 1988b). In contrast, stimulation of 5-HT 1A receptors by ipsapirone was followed by an attenuated hypothermic and ACTH/cortisol response in patients with PDA (Broocks et al. 2000;Lesch et al. 1992). In healthy controls, ipsapirone produces dose-dependent increases in plasma cortisol and ACTH as well as dose-dependent reductions in body temperature (Cowen 2001;Kahn et al. 1994;Lesch et al. 1989). Ipsapirone acts on specific serotonergic mechanisms in the brain through its high-affinity binding to the 5-HT 1A receptor subtype. The binding sites are predominantly located on serotonergic neurons in the raphe nuclei (presynaptic autoreceptors) and in limbic structures (postsynaptic receptors). Agonistic properties at presynaptic somatodendritic sites have been observed, resulting in decreased serotonergic neurotransmission (Peroutka 1985). Concerning the high selectivity of ipsapirone, it has to be considered that the metabolite 1-(2-pyrimidinyl)-piperazine (1-PP) has been found to exert antagonistic effects at pre-and postsynaptic ␣ 2-adrenoceptors (Blier et al. 1991;Miller et al. 1992).Several lines of evidence suggest that serotonergic neurotransmission, including the regulation of 5-HT1A receptors, is affected by nicotine (Benwell et al. 1990;Kenny et al. 2001). Recent studies show that some of nicotine's psychotropic and endocrine effects are exerted by stimulation of 5-HT1A receptors on dorsal raphe neurons (Cheeta et al. 2001;Mihailescu et al. 2001).There is a high incidence of smoking in patients with anxiety and other psychiatric disorders (Breslau et al. 1993;Glassman 1993;Kendler et al. 1993;Marks et al. 1997;Miller and Gold 1998;Sellman et al. 1999). To our knowledge, no clinical studies have examined the question of whether psychological or neurobiological effects induced by serotonergic agents such as ipsapi...

show abstract

Adrenergic Function in Patients With Panic Anxiety

Cited by 250 publications

References 54 publications

Psychological States and Lymphocyte β-Adrenergic Receptor Responsiveness

Psychological States and Lymphocyte β-Adrenergic Receptor Responsiveness

Neural Pathways Underlying Lactate-Induced Panic

Smoking Modulates Neuroendocrine Responses to Ipsapirone in Patients with Panic Disorder

Contact Info

Product

Resources

About