Adrenergic status in anxiety disorders: Platelet alpha2-adrenergic receptor binding, blood pressure, pulse, and plasma catecholamines in panic and generalized anxiety disorders patients and in normal subjects

Abstract

In order to evaluate adrenergic function in anxiety disorders, platelet alphaz-adrenergic binding parameters and supine and standing blood pressure, pulse, and venous plasma epinephrine and norepinephrine were determined in patients with panic attaclcs or generalized anxiety disorder arm in normal subjects. The maximum number of binding sites (Bm,~) for the partial agonist tritiated cionidine was significantly lower for both patient groups than for normal subjects, and the Bm~for the antagonist tritiated yohimbine was significantly lower for panic patients. There were no other substantive differences across groups. Prior exposure to psychotropic drugs might account for the results for clonidine binding, but not for yohimbine. The Bm~for clonidine w~ls eorrelated with norepinephrine increases upon standing and, for panic patients, with tl~e severity of fuU unexpected panic attacks. These data provide further evidence of adtenergic receptor abnormalities in people with anxiety disorders.

Symptom dimensions of anxiety following myocardial infarction: Associations with depressive symptoms and prognosis.

“…Anxiety is potentially related to various pathophysiological processes in patients with MI, including increased risk of ventricular arrhythmias [Watkins et al 2006], reduced heart rate variability (HRV) [Martens et al 2008], inflammatory processes [Pitsavos et al 2006], increased platelet activity [Cameron et al 1990] and HPA axis dysregulation [Vreeburg et al 2010].…”

Noradrenergic mechanisms in stress and anxiety: II. Clinical studies

“…This can take the form, for instance, of worrying about one's finances, misfortune to one's children when there is no danger present, or problems with one's health when there is no cause for concern. Plasma MHPG levels have been Behavioral and bioloeical effects of vohimbine Sevy et al, 1989;Mathew Mathew et al, 1980Sevy et al, 1989Munjack et al, 1990Mathew et al, 1981Sevy et al, 1989Curtis et al, 1989Munjack et al, 1990Cameron et al, 1990Charney et al, 1987bNesse et al, 1985bStein et al, 1992 Tancer and Siever et al, 1983Siever et al, 1983 Siever et al, Lee et al, 1990Curtis et al, 1989Hollander et al, 1991;Lee et al, 1990 shown to be increased in GAD patients in comparison to normal controls (Munjack et al, 1990;Sevy et al, 1989), while conflicting results have been obtained for resting plasma norepinephrine (Table IV). Other studies have shown an increase in plasma epinephrine in comparison to controls (Mathew et al, 1980(Mathew et al, , 1981.…”

“…Patients with panic disorder have been found to have a decrease in peripheral lymphocyte p-adrenergic binding sites (B,,,=) and in increase in affinity (KD) (Brown et al, 19881, as well as a decrease in basal activity of cyclic adenosine monophosphate (CAMP), a second Refuting Nesse et al, 1984, 198513;Cameron and Nesse, 1988;Gorman et al, 1988;Freedman et al, 1984Gorman et al. 1988Charney et al, 1987aStein et al, 1992Woods et al, 1987Freedman et al, 1985;Taylor et al, 1986;Shear et al, 1987;Balon et al, 1988Balon et al, 1988White andBaker, Nesse et al, 1985b Nesse et al, 1984;Villacres et al, 1987 Cameron et al, 198413;Nesse et al, 1985aKO et al, 1983Brown et al, 1988Charney et al, 1990Cameron et al, 1990Cameron et al, 1984, 1990Albus et al, 1986 Charney et al, 1990a Uhde et al, 1984Uhde et al, , 1989Liebowitz et al, Uhde et al, 1986;Charney and 1981;Hoehn-Saric et al, 1981Heninger, 1986Curtis et al, 1989;Charney et al, 1992Charnev et al, 1984a, 1987a: Uhde Freedman et al, 1985Cameron et al, 1987;Villacres et al, 1987;Stein et al, 1992…”

The Association of Urinary 5-Hydroxyindoleacetic Acid and Vanillylmandelic Acid in Patients with Generalized Anxiety

“…Sevy et al [19] found that plas ma N E and one of its metabolites, 3-methoxy-4-hydroxyphenylglycol, were increased in G A D compared to con trols. Cameron et al [20] reported that G A D patients had reduced NE receptor binding. If 5-HT and NE are associ ated in some way with the pathophysiology of G A D , then there could be a relationship between the metabolites of these neurotransmitters.…”

“…The possible involvement of 5-HT in generalized anxiety is suggested by various pharmaco logical investigations. Many patients with G A D respond favorably to the 5-HT 1A agonists buspirone [3] and gepirone [4], and to the 5-HT and norepinephrine (NE) reup take blocker, imipramine [5], The 5-HT 2 antagonist ritanserin appears to be effective at reducing general anxi ety [6], The 5-HT agonist, m-chlorophenylpiperazine (m-CPP), causes anxiety in panic patients and healthy con trols [7,8].There are also substantial data implicating NE in volvement in anxiety [9-23], However, not all studies of catecholamines in G A D show differences between G A D patients and controls [ 17,22,24], There are additonal data from investigations of panic disorder suggesting abnormalities of 5-HT [1,2], and NE metabolism [1,20,[25][26][27][28][29][30] may be involved in some way with the pathophysiology of anxiety. It is unclear whether these biochemical findings in panic disorder are true for G A D .…”