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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether perinatal complications predict childhood anxiety disorders independently of parental psychopathology, we systematically assessed pregnancy and delivery complications and psychopathology in a sample of children (mean age=6.8 years) at high risk for anxiety disorders whose parents had panic disorder with (n=138) or without (n=26) major depression, and in contrast groups of offspring of parents with major depression alone (n=47), or no mood or anxiety disorders (n=95; total N=306). Psychopathology in the children was assessed by structured diagnostic interviews (K-SADS), and pregnancy and delivery complications were assessed using the developmental history module of the DICA-P. Number of pregnancy complications predicted multiple childhood anxiety disorders independently of parental diagnosis (odds ratio=1.6 [1.4-2.0]). This effect was accounted for by heavy bleeding requiring bed-rest, hypertension, illness requiring medical attention, and serious family problems. Associations remained significant when lifetime child mood and disruptive behavior disorders were covaried. Results suggest that prenatal stressors may increase a child's risk for anxiety disorders beyond the risk conferred by parental psychopathology alone.
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PMID:Pregnancy complications associated with childhood anxiety disorders. 1512 17

The ability of serotonin (5-HT) to facilitate or attenuate autonomic, endocrine, and behavioral responses to stressful stimuli has received much attention. The effects of 5-HT on physiologic and behavioral responses to stressful stimuli seem to depend on the brain region where it is released and the effector system it acts upon. This and the distinct morphology and topographic organization of subpopulations of serotonergic neurons have led to the hypothesis that subpopulations of serotonergic neurons are functionally distinct. Serotonin's role as a modulator of the "fight-or-flight" response is mediated in part by 5-HT release in the dorsolateral periaqueductal gray (DLPAG) and in the rostral ventrolateral medulla (RVLM), an area that contains sympathoexcitatory C1 adrenergic (A) neurons. The release of 5-HT in either region inhibits stress-induced sympathetic activity in part via actions on 5-HT(1A) receptors. In addition, 5-HT release in the DLPAG inhibits fight-or-flight or "Go" behaviors. The origin of endogenous 5-HT in the DLPAG and RVLM seems to be a subpopulation of serotonergic neurons within the ventrolateral PAG, a region implicated in "freezing" or "No Go" behaviors. These serotonergic neurons are located in the lateral "wings" of the dorsal raphe nucleus (DRN) a region also referred to as the ventrolateral DRN. The existence of a functional subpopulation of serotonergic neurons capable of inhibiting sympathoexcitation and fight-or-flight behavioral responses may be clinically relevant for explaining in part the efficacy of serotonergic drugs in the treatment of hypertension and panic attacks in panic disorder patients.
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PMID:A functional subset of serotonergic neurons in the rat ventrolateral periaqueductal gray implicated in the inhibition of sympathoexcitation and panic. 1524 Mar 52

There is a plausible biological basis for the association between psychiatric morbidity and cardiovascular disease. Anxiety, panic disorder, and depression are common in patients with coronary heart disease and hypertension. Despite this evidence there is poor recognition of anxiety disorders and depression in primary care and hospital medical practice. Concern also surrounds the use of psychotropic drugs in patients with cardiovascular disease. In the first of the two articles on this subject, we highlighted the current evidence regarding the association between cardiovascular and psychotropic conditions. In this second article, we discuss the interaction of the drugs used in the management of these two varied but commonly coexistent group of diseases as well as their relative effects on either system. Finally, we summarise the data regarding the safe use of these medications based on the recommendations from the currently available evidence.
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PMID:Heart and mind: (2) psychotropic and cardiovascular therapeutics. 1564 Apr 26

Panic disorder (PD) is an acute psychobiologic reaction manifested by intense anxiety and panic attacks, that occur unpredictably with subjective sense of intense apprehension or terror, accompanied by temporary loss of the ability to plan, think, or reason and the intense desire to escape or flee the situation. Panic attacks may last from a few seconds to an hour or longer. Symptoms typically include, among others, palpitations, tachycardia, hypertension, chest pain, dyspnoea, and fear of loosing control or going crazy and vague feeling of imminent doom or death. Since pharmacotherapy of PD includes the administration of selective serotonin reuptake inhibitors and tricyclic antidepressants, the objective of this study was to perform a pilot double blind clinical trial designed to compare the effects of two studied drugs in the treatment of PD. A total number of 40 patients with a history of panic disorder were randomly assigned into two groups of 20 patients each. Hamilton anxiety rating scale and Standard Psychiatric Interview were methods for PD assessment. One group was treated with clomipramine hydrochloride (ANAFRANIL) 75 mg/day and the other with fluoxetine (OXETIN) 60 mg/day. Both drugs were administrated by mouth (PO) two times-a-day in equally divided doses for 6 weeks. Both studied agents produced similar antipanic effectiveness. Favourable response was achieved in 95% of patients treated with fluoxetine and 90% of patients treated with clomipramine. The onset of antipanic effects was quicker in all clomipramine treated patients, while fluoxetine produced more-favourable response in male patients. The duration of treatment with both antidepressants studied should be at least 10 weeks, instead of 6 weeks.
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PMID:Clomipramine and fluoxetine effects in the treatment of panic disorder. 1623 46

The most frequently occurring pre- and postpartum psychiatric disorders are depression and, to a lesser degree, panic disorder and psychosis. Apart from the negative effects on the psychological well-being of the mother, these psychiatric disorders may also result in obstetric complications and an impaired mother-infant relationship. In order to prevent these negative effects, mothers who are at risk for major psychiatric disorders need to be identified early, preferably before or during pregnancy. The most important risk factor is a history of psychiatric disorders. Obstetric risk factors for depression are unplanned or unwanted pregnancy, pregnancy-related hypertension, emergency caesarean section and early discharge from the hospital. Other factors are low socioeconomic status, recent life event, negative self-image, little social support, immigration in the last 5 years, feelings of loss of control during pregnancy and feeding problems with the child. For treatment, pregnant or puerperal women with a possible psychiatric disorder based on the presence of a serious risk factor, such as a previously experienced psychiatric disorder (related to pregnancy or not), serious current psychiatric symptoms or long-time use of psychoactive drugs, should be referred preferably to a combined psychiatric/obstetric clinic or, if unavailable, to a psychiatrist in a general hospital.
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PMID:[Psychiatric disorders in pregnant and puerperal women]. 1667 19

When venlafaxine was introduced in 1994, it was the first of the newer generation antidepressants to be classified as a serotonin norepinephrine reuptake inhibitor (SNRI). An extended release (XR) formulation of venlafaxine, introduced in 1997, subsequently received regulatory approval for treatment of three anxiety disorders: generalized anxiety disorder, social anxiety disorder and panic disorder. Although less extensively studied, venlafaxine XR also appears to have efficacy for two other anxiety disorders, post-traumatic stress disorder and obsessive-compulsive disorder. In contrast to the treatment of depression, for which meta-analyses suggest an efficacy advantage relative to selective serotonin reuptake inhibitors (SSRIs), evidence of differential efficacy has not yet been established for any of the anxiety disorders. The overall tolerability profile of venlafaxine XR is generally comparable to that of the SSRIs, although there is greater incidence of noradrenergically mediated side effects (i.e., dry mouth and constipation), as well as a dose-dependent risk of treatment-emergent high blood pressure. Concerns about safety in overdose have also recently emerged. Despite these caveats, venlafaxine XR is an effective and generally well-tolerated option for treatment of anxiety disorders.
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PMID:Treatment of anxiety disorders with venlafaxine XR. 1653 31

Rats with chronic inhibition of GABA synthesis and consequently enhanced glutamatergic excitation in the dorsomedial hypothalamus (DMH) develop panic-like responses, defined as tachycardia, tachypnea, hypertension, and increased anxiety as measured by a social interaction (SI) test, after intravenous sodium lactate infusions, a phenomenon similar to patients with panic disorder. Therefore, the present studies tested the role of the postsynaptic NMDA and AMPA type glutamatergic receptors in the lactate-induced panic-like responses in these rats. Rats were fit with femoral arterial and venous catheters and Alzet pumps [filled with the GABA synthesis inhibitor L-allylglycine (L-AG; 3.5 nmol/0.5 microl per hour) or its inactive isomer D-AG] into the DMH. After 4-5 d of recovery only those rats with L-AG pumps exhibited panic-like responses to lactate infusions. Using double immunocytochemistry, we found that rats exhibiting panic-like responses (e.g., L-AG plus lactate) had increased c-Fos immunoreactivity in DMH neurons expressing the NMDA receptor 1 (NR1) subunit, but not those expressing the glutamate receptor 2 and 3 subunits of the AMPA receptors. To confirm this pharmacologically, we tested another group of rats implanted with l-AG pumps with intravenous lactate infusions preceded by injections of either NMDA [aminophosphonopentanoic acid (AP-5) or (+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d]cyclohepten-5,10-imine maleate (MK-801)] or non-NMDA [CNQX or 4-(8-methyl-9H-1,3-dioxolo[4,5-h][2,3]benzodazepin-5-yl)-benzenamine dihydrochloride (GYKI52466)] antagonists into the DMH. Injections of NMDA, but not non-NMDA, antagonists into the DMH resulted in dose-dependent blockade of the tachycardia, tachypnea, hypertension, and SI responses after lactate infusions. These results suggest that NMDA, and not non-NMDA, type glutamate receptors regulate lactate-induced panic-like responses in rats with GABA dysfunction in the DMH.
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PMID:Panic-prone state induced in rats with GABA dysfunction in the dorsomedial hypothalamus is mediated by NMDA receptors. 1680 38

Intravenous sodium lactate infusions or the noradrenergic agent yohimbine reliably induce panic attacks in humans with panic disorder but not in healthy controls. However, the exact mechanism of lactate eliciting a panic attack is still unknown. In rats with chronic disruption of GABA-mediated inhibition in the dorsomedial hypothalamus (DMH), achieved by chronic microinfusion of the glutamic acid decarboxylase inhibitor L-allylglycine, sodium lactate infusions or yohimbine elicits panic-like responses (i.e., anxiety, tachycardia, hypertension, and tachypnea). In the present study, previous injections of the angiotensin-II (A-II) type 1 receptor antagonist losartan and the nonspecific A-II receptor antagonist saralasin into the DMH of "panic-prone" rats blocked the anxiety-like and physiological components of lactate-induced panic-like responses. In addition, direct injections of A-II into the DMH of these panic-prone rats also elicited panic-like responses that were blocked by pretreatment with saralasin. Microinjections of saralasin into the DMH did not block the panic-like responses elicited by intravenous infusions of the noradrenergic agent yohimbine or by direct injections of NMDA into the DMH. The presence of the A-II type 1 receptors in the region of the DMH was demonstrated using immunohistochemistry. Thus, these results implicate A-II pathways and the A-II receptors in the hypothalamus as putative substrates for sodium lactate-induced panic-like responses in vulnerable subjects.
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PMID:Angiotensin-II is a putative neurotransmitter in lactate-induced panic-like responses in rats with disruption of GABAergic inhibition in the dorsomedial hypothalamus. 1695 77

1. In searching for biological evidence that essential hypertension is caused by chronic mental stress, a disputed proposition, parallels are noted with panic disorder, which provides an explicit clinical model of recurring stress responses. 2. There is clinical comorbidity; panic disorder prevalence is increased threefold in essential hypertension. Plasma cortisol is elevated in both. 3. In panic disorder and essential hypertension, but not in health, single sympathetic nerve fibres commonly fire repeatedly within an individual cardiac cycle; this appears to be a signature of stress exposure. For both conditions, adrenaline cotransmission is present in sympathetic nerves. 4. Tissue nerve growth factor is increased in both (nerve growth factor is a stress reactant). There is induction of the adrenaline synthesizing enzyme, phenylethanolamine-N-methyltransferase, in sympathetic nerves, an explicit indicator of mental stress exposure. 5. The question of whether chronic mental stress causes high blood pressure, still hotly debated, has been reviewed by an Australian Government body, the Specialist Medical Review Council. Despite the challenging medicolegal implications, the Council determined that stress is one proven cause of hypertension, this ruling being published in the 27 March 2002 Australian Government Gazette. This judgement was reached after consideration of the epidemiological evidence, but in particular after review of the specific elements of the neural pathophysiology of essential hypertension, described above.
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PMID:Chronic mental stress is a cause of essential hypertension: presence of biological markers of stress. 1830 49

This paper reviews the limited literature on paroxysmal hypertension. A case report describes the clinical picture frequently seen in specialty hypertension practice, a patient with paroxysmal or intermittent hypertension who proves not to have a pheochromocytoma. The variety of diagnostic labels given to these patients is reviewed, including pseudopheochromocytoma, panic attacks, and hyperventilation syndrome. The clinical features, pathology, diagnosis, and treatment of these syndromes are outlined. It is proposed that successful management of these patients may be best achieved by collaborative care between a hypertension specialist and a psychiatrist or clinical psychologist with expertise in cognitive-behavioral panic management, stress-reduction techniques including controlled breathing, and treating health anxiety. The use of drugs effective for treatment of panic disorder can also be helpful in managing these patients.
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PMID:Paroxysmal hypertension: the role of stress and psychological factors. 1860 43


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