Effects of SSRI medication on heart rate and blood pressure in individuals with hypertension and depression.

OBJECTIVE: To test the role of escitalopram on blood pressure and heart rate of individuals with hypertension and depression. METHODS: A total of 30 individuals participated in this study who were being treated for hypertension and were diagnosed with major depression. Escitalopram (10-20 mg) was administered to 15 individuals, while the other 15 received placebo. These individuals were followed for 8 weeks with regular monitoring of blood pressure and heart rate. Scores on the Hamilton Depression Rating Scale were evaluated within the first, second, fourth, and eighth weeks of the study onset. RESULTS: Comparing with placebo, heart rate was lower in the escitalopram group (66.79 ± 9.85 vs. 74.10 ± 9.52 bpm, p = 0.044). There was not a significant decrease of systolic blood pressure (140.80 ± 16.48 vs 139.61 ± 18.92 mmHg, p = 0.85) and diastolic blood pressure (80.55 ± 12.64 vs 80.18 ± 16.36 mmHg, p = 0.94). CONCLUSION: Escitalopram decreases HR, but not BP, in individuals with hypertension and depression. Abbreviation: SH: systemic hypertension; BP: blood pressure; DSM: Diagnostic and Statistical Manual of Mental Disorders; SRQ 20: Self-Report Questionnaire; SCID: Structured Clinical Interview for DSM-IV; HR: heart rate; SNS: Sympathetic nervous system; HPA: hypothalamus-pituitary-adrenal axis; RAA: renin, angiotensin, aldosterone system; NE: norepinephrine; CSF: cerebrospinal fluid; HAM-D: Hamilton Depression Rating Scale; CRF: corticotropin releasing factor; ACTH: adrenocorticotropic hormone; BMI: Body mass index; SBP: systolic blood pressure; DBP: diastolic blood pressure; t: time.

Don't panic. A guide to tryptophan depletion with disorder-specific anxiety provocation.

The 2002 paper "Does 5-HT restrain panic? A tryptophan depletion study in panic disorder patients recovered on paroxetine" by Bell and colleagues - reprinted in this issue of the Journal - reports on a study undertaken in the halcyon days of David Nutt's Psychopharmacology Unit at the University of Bristol, England. In this invited commentary authors of the original work discuss the impact of this paper on the field of acute tryptophan depletion research (especially in the field of clinical anxiety disorders) and the development of disorder-specific anxiogenic provocations over the past decade.

Noradrenergic function in generalized anxiety disorder: impact of treatment with venlafaxine on the physiological and psychological responses to clonidine challenge.

Serotonin and noradrenaline reuptake inhibitor (SNRI) antidepressants have evidence of efficacy in the treatment of generalized anxiety disorder (GAD); however, it is not clear whether there is an advantage over selective serotonin reuptake inhibitor (SSRI) medicines and there is limited evidence for noradrenergic dysfunction in GAD. We tested whether a dysfunctional alpha-2 adrenoceptor system is present in patients with GAD and the effects of SNRI treatment on this system. The method used was an infusion of clonidine (a selective alpha-2 adrenergic receptor agonist) on psychological and physiological outcomes in three subject groups: 10 untreated GAD patients, five SNRI-treated GAD patients and seven normal controls. The clonidine challenge elicited sedation, a rise in growth hormone, decrease in blood pressure, decline in saccadic eye movement (SEM) variables, and improvement in verbal fluency as anticipated in the 22 subjects examined. Lower cortisol levels were found in controls and higher blood pressure readings in GAD-treated subjects, as well as evidence that GAD-treated subjects had SEMs that were intermediate between control and GAD subjects' scores and have less clonidine-induced sedation. The implications of these findings with reference to the study hypothesis in this small study are discussed.

Dopaminergic challenges in social anxiety disorder: evidence for dopamine D3 desensitisation following successful treatment with serotonergic antidepressants.

Serotonergic antidepressants (SSRIs) are first-line treatments for social anxiety disorder [SAnD], though there is evidence of dopaminergic system dysfunction. Twenty subjects with DSM-IV SAnD, untreated (n = 10) and SSRI-remitted DSM-IV SAnD (n = 10), were administered a single dose of 1) a dopamine agonist (pramipexole 0.5 mg) and 2) a dopamine antagonist (sulpiride 400 mg), followed by anxiogenic challenges (verbal tasks and autobiographical scripts) in a double-blind crossover design, the two test days being one week apart. Anxiety symptoms were measured by self-reported changes in Visual Analogue Scales, specific SAnD scales and anxiety questionnaires. Plasma levels of prolactin were obtained. Untreated SAnD subjects experienced significant increases in anxiety symptoms following behavioural challenges after either sulpiride or pramipexole. Following remission with SSRIs, the socially anxiogenic effect of behavioural provocation was significantly attenuated under pramipexole, whereas under sulpiride effects remained significantly elevated. There appears to be instability of the dopamine system under behavioural stress in social anxiety subjects that is only partly rectified by successful treatment with an SSRI, which may induce a desensitisation of postsynaptic dopamine D(3) receptors.