Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies have shown unequivocally a lack of pituitary-adrenocortical stress hormone activation during lactate-induced panic attacks despite considerable psychopathological alterations, signs of arousal and several vegetative symptoms regularly occurring during stressful conditions. To study the possible inhibitory action of atrial natriuretic hormone (ANH) on adrenocorticotrophic hormone (ACTH) and cortisol release in humans, 10 patients with panic disorder (DSM-III-R) received sodium lactate and placebo (0.9% saline) infusions and ten healthy comparison subjects additionally received a 2.5% saline infusion and the response of ANH, vasopressin, ACTH, cortisol, and several biochemical and physiological cardiovascular parameters were measured. In comparison to placebo, lactate infusion led to enhanced ANH levels in both non-panicking comparison subjects and panickers. Importantly, panickers showed significantly lower baseline levels of ANH than comparison subjects followed by a faster release. No significant concomitant changes in vasopressin, ACTH, and cortisol were observed. During lactate infusion, heart rate was accelerated considerably in the two groups; in contrast, the reduction of pCO2 indicated an enhanced ventilation only in panickers. The pattern of ANH release cannot be attributed simply to either the volume load administered, the cardiac activation or an osmotic effect since neither 0.9 nor 2.5% saline resulted in comparable effects. Additional central nervous mechanisms must be considered for the increased ANH concentrations in lactate-induced panic attacks. We propose that the release of ANH is an intrinsic mechanism contributing to the apparent unresponsiveness of the pituitary-adrenocortical system in lactate-induced panic attacks. In addition, we surmise that ANH may also play a role in the yet unknown mechanisms for termination of panic attacks, e.g. either by inhibitory actions on the locus coeruleus or by bronchiorelaxation and consecutive decatastrophization.
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PMID:Atrial natriuretic hormone in lactate-induced panic attacks: mode of release and endocrine and pathophysiological consequences. 969 99

We enrolled six patients suffering from refractory chronic cluster headache in a pilot trial of neurostimulation of the ipsilateral ventroposterior hypothalamus using the stereotactic coordinates published previously. After the varying durations needed to determine optimal stimulation parameters and a mean follow-up of 14.5 months, the clinical outcome is excellent in three patients (two are pain-free; one has fewer than three attacks per month), but unsatisfactory in one patient, who only has had transient remissions. Mean voltage is 3.28 V, diplopia being the major factor limiting its increase. When the stimulator was switched off in one pain-free patient, attacks resumed after 3 months until it was turned on again. In one patient the implantation procedure had to be interrupted because of a panic attack with autonomic disturbances. Another patient died from an intracerebral haemorrhage that developed along the lead tract several hours after surgery; there were no other vascular changes on post-mortem examination. After 1 month, the hypothalamic stimulation induced resistance against the attack-triggering agent nitroglycerin and tended to increase pain thresholds at extracephalic, but not at cephalic, sites. It had no detectable effect on neurohypophyseal hormones or melatonin excretion. We conclude that hypothalamic stimulation has remarkable efficacy in most, but not all, patients with treatment-resistant chronic cluster headache. Its efficacy is not due to a simple analgesic effect or to hormonal changes. Intracerebral haemorrhage cannot be neglected in the risk evaluation of the procedure. Whether it might be more prevalent than in deep-brain stimulation for movement disorders remains to be determined.
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PMID:Hypothalamic stimulation in chronic cluster headache: a pilot study of efficacy and mode of action. 1568 58