Increased pulse and blood pressure associated with desipramine treatment of bulimia nervosa.
ABSTRACT The cardiovascular effects of desipramine were assessed in 74 young women with bulimia nervosa participating in a 6-week double-blind, placebo-controlled study. Desipramine treatment was associated with significant increases in pulse, reclining systolic and diastolic blood pressures, and orthostatic hypotension. These effects were clearly evident in the first week of treatment and remained relatively unchanged during the subsequent 5 weeks. The mean increases in reclining systolic and diastolic pressures were approximately 10 mm Hg. Data from 16 patients treated for an additional 2 months indicated that most of the effects of desipramine on blood pressure diminished over time, whereas the effects on pulse persisted. These results differ from the commonly expected cardiovascular effects of tricyclic anti-depressants in adults. Evidence from the current study and from other reports suggests that the cardiovascular effects of tricyclic antidepressants are age-dependent.
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ABSTRACT: Orthostatic intolerance (OI) or postural tachycardia syndrome (POTS) is a syndrome primarily affecting young females, and is characterized by lightheadedness, palpitations, fatigue, altered mentation, and syncope primarily occurring with upright posture and being relieved by lying down. There is typically tachycardia and raised plasma norepinephrine levels on upright posture, but little or no orthostatic hypotension. The pathophysiology of OI is believed to be very heterogeneous. Most studies of the syndrome have focused on abnormalities in norepinephrine release. Here the hypothesis that abnormal norepinephrine transporter (NET) function might contribute to the pathophysiology in some patients with OI was tested. In a proband with significant orthostatic symptoms and tachycardia, disproportionately elevated plasma norepinephrine with standing, impaired systemic, and local clearance of infused tritiated norepinephrine, impaired tyramine responsiveness, and a dissociation between stimulated plasma norepinephrine and DHPG elevation were found. Studies of NET gene structure in the proband revealed a coding mutation that converts a highly conserved transmembrane domain Ala residue to Pro. Analysis of the protein produced by the mutant cDNA in transfected cells demonstrated greater than 98% reduction in activity relative to normal. NE, DHPG/NE, and heart rate correlated with the mutant allele in this family. CONCLUSION: These results represent the first identification of a specific genetic defect in OI and the first disease linked to a coding alteration in a Na+/Cl(-)-dependent neurotransmitter transporter. Identification of this mechanism may facilitate our understanding of genetic causes of OI and lead to the development of more effective therapeutic modalities.Annals of the New York Academy of Sciences 07/2001; 940:527-43. · 3.15 Impact Factor
Article: Depression is associated with decreased blood pressure, but antidepressant use increases the risk for hypertension.[show abstract] [hide abstract]
ABSTRACT: The present study compared blood pressure levels between subjects with clinical anxiety and depressive disorders with healthy controls. Cross-sectional data were obtained in a large cohort study, the Netherlands Study of Depression and Anxiety (N=2981). Participants were classified as controls (N=590) or currently or remittedly depressed or anxious subjects (N=2028), of which 1384 were not and 644 were using antidepressants. Regression analyses calculated the contributions of anxiety and depressive disorders and antidepressant use to diastolic and systolic blood pressures, after controlling for multiple covariates. Heart rate and heart rate variability measures were subsequently added to test whether effects of anxiety/depression or medication were mediated by vagal control over the heart. Higher mean diastolic blood pressure was found among the current anxious subjects (beta=0.932; P=0.03), although anxiety was not significantly related to hypertension risk. Remitted and current depressed subjects had a lower mean systolic blood pressure (beta=-1.74, P=0.04 and beta=-2.35, P=0.004, respectively) and were significantly less likely to have isolated systolic hypertension than controls. Users of tricyclic antidepressants had higher mean systolic and diastolic blood pressures and were more likely to have hypertension stage 1 (odds ratio: 1.90; 95% CI: 0.94 to 3.84; P=0.07) and stage 2 (odds ratio: 3.19; 95% CI: 1.35 to 7.59; P=0.008). Users of noradrenergic and serotonergic working antidepressants were more likely to have hypertension stage 1. This study shows that depressive disorder is associated with low systolic blood pressure and less hypertension, whereas the use of certain antidepressants is associated with both high diastolic and systolic blood pressures and hypertension.Hypertension 03/2009; 53(4):631-8. · 6.21 Impact Factor