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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The onset of therapeutic effectiveness of carbamazepine is generally very rapid in the treatment of seizure and paroxysmal pain disorders, shows some lag in the treatment of mania, and exhibits the longest lag in depression. These time course variations may indicate that different mechanisms underlie the efficacy of carbamazepine in the differential neuropsychiatric syndromes. Biochemical and pharmacological data suggest that the anticonvulsant effects of carbamazepine are related to "peripheral-type" benzodiazepine and alpha 2-noradrenergic receptor systems and to its ability to stabilize sodium channels. GABAB (baclofen-like) actions appear to be involved in antinociceptive, but not anticonvulsant, effects. The relatively acute time course of antimanic efficacy may be related to the above-mentioned mechanisms or to other effects related to systems postulated to be altered in the manic syndrome. These effects might include carbamazepine's ability to increase acetylcholine in the striatum, decrease probenecid-induced levels of CSF homovanillic acid (HVA) in man and dopamine turnover in animals, decrease CSF norepinephrine in manic patients, inhibit adenylate cyclase activity (in response to norepinephrine, dopamine, adenosine, or ouabain), decrease GABA turnover, or act as a vasopressin agonist. Efficacy in depression may be related to actions in man that take time or chronic drug administration to develop, such as increases in plasma tryptophan, decreases in CSF somatostatin, decreases in thyroid indices, and increases in urinary free cortisol excretion and, in animals, increases in substance P sensitivity and increases in brain adenosine receptors. The ability of carbamazepine to block the development of lidocaine- and cocaine-induced seizures also requires chronic administration, suggesting that these seizure models may provide a unique perspective for understanding mechanisms of time-dependent effects.
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PMID:Time course of clinical effects of carbamazepine: implications for mechanisms of action. 328 May 60

Fourteen Alzheimer subjects participated in a parallel group study of desamino-D-arginine-vasopressin (DDAVP, desmopressin). All subjects received one week of single-blind placebo. Then on a double-blind basis, the active group received DDAVP intranasally in doses starting at 30 micrograms per day and increasing over a 3 week period to 180 micrograms per day; the control group received an identical placebo. Using a repeated measures ANOVA, three measures out of thirty-one were found to be statistically significant for DDAVP treatment: the Hamilton depression scale and the affect and interpersonal subscales of the SCAG. However, the magnitude of these changes was probably too small to be clinically significant. Except for one subject who transiently became hyponatremic (Na of 120) and confused while receiving 180 micrograms of DDAVP, there were no adverse effects. There were no significant group changes in sodium, potassium, plasma osmolality, blood pressure, and weight.
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PMID:Desamino-D-arginine-vasopressin (DDAVP) in Alzheimer's disease. 352 91

We have previously demonstrated that chronic intracerebroventricular (ICV) administration of captopril attenuates the development of hypertension in young SHR in association with a depression in whole animal reactivity to vasoactive agents and an increased baroreflex sensitivity. In the present study we analyzed vascular reactivity in perfused kidneys from SHR treated with captopril or vehicle to determine whether the depression in reactivity was due to changes in baroreflex activity or an effect on the vasculature. Captopril (1.25 micrograms/hr) was infused (osmotic mini pumps) for 4 weeks. Vascular reactivity to norepinephrine, angiotensin and vasopressin was assessed in isolated kidneys perfused with an artificial medium at constant flow. SHR treated with ICV captopril showed a significantly lower arterial pressure and basal renal vascular resistance than SHR treated with ICV vehicle or IV captopril. In addition, these rats showed decreased vascular reactivity to all vasoactive agents tested as signified by a shift in the dose-response curves to the right with an increase in threshold (ED16) and ED50. Kidneys from WKY treated with ICV captopril also showed a decrease in vascular reactivity in comparison to WKY treated with ICV vehicle. Our data suggest that captopril, through a central action, attenuates the development of hypertension by decreasing vascular reactivity to vasoconstrictors.
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PMID:Alterations in renal vascular reactivity induced by chronic central administration of captopril in the spontaneously hypertensive rat. 353 26

Rats were treated with Escherichia coli endotoxin (ET) either acutely or chronically or rendered septic by cecal ligation and puncture. At 6 h after ET injection, at various intervals of continuous ET infusion, and at 17-18 h after the onset of peritonitis, animals were killed and hepatocytes were isolated. Cytosolic [Ca2+] ([Ca2+]c) was measured by quin 2 during the resting state and after stimulation with epinephrine and vasopressin. Basal and epinephrine-, vasopressin- and glucagon-stimulated glycogen phosphorylase activity were also determined. In hepatocytes from acutely ET-treated rats, resting levels of [Ca2+]c were decreased 46% from 245.8 +/- 11.0 to 131.0 +/- 8.5 nM (n = 4-6, P less than 0.05). In septic rats a 39.5% decrease was noted [i.e., from 154.0 +/- 17.7 (n = 4, sham) to 93.3 +/- 91 nM (n = 5, septic, P less than 0.05)]. These decreased [Ca2+]c levels were associated with changes of glycogen phosphorylase activity in a manner suggesting a cause and effect relationship; e.g., acute ET treatment resulted in greater than 80% depression of phosphorylase a activity, whereas sepsis induced a 58% decrease in the activity of this enzyme. In ET-infused rats the resting level of [Ca2+]c and its response to hormonal stimulation were not different from hepatocytes of saline-infused rats, although glycogen phosphorylase activity was less responsive to these hormones. The effect on the enzyme's response to Ca2+-mobilizing hormones was more marked than to glucagon. This is consistent with the concept that information flow in the Ca2+-messenger system is a site of metabolic lesions produced by endotoxicosis and sepsis.
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PMID:Rat liver free cytosolic Ca2+ and glycogen phosphorylase in endotoxicosis and sepsis. 353 41

1. Extracellular recordings in pentobarbitone anaesthetized male Long-Evans rats examined the influence of electrical stimulation in the diagonal band of Broca on the excitability of 113 putative vasopressin-secreting and 22 putative oxytocin-secreting neurosecretory neurones in the hypothalamic supraoptic nucleus. 2. Single pulse or repetitive (5-20 Hz) stimulation in the ventral part of the diagonal band evoked a prominent reduction in the excitability of 83% of vasopressin-secreting neurones with no effect on the remainder. Amongst oxytocin-secreting neurones, 59% were unresponsive, 27% responded with an increase in activity while only 14% revealed an inhibitory pattern similar to vasopressin-secreting neurones. 3. Diagonal band stimulation-evoked inhibitions were reversibly abolished by local pressure applications of bicuculline methiodide (100 microM) to twenty out of twenty vasopressin secreting cells tested, whereas strychnine sulphate (100 microM) was without effect on four out of four cells tested. 4. In five out of five vasopressin-secreting cells tested, bicuculline applications reversibly abolished the reduction in their activity that follows peripheral baro-receptor activation. Failure to alter baroreflex-evoked depressions in firing during similar trials with prazosin hydrochloride (10 microM, six cells tested), timolol maleate (20 microM, six cells tested) or strychnine sulphate (100 microM, three cells tested) indicated the specificity of bicuculline's action. 5. These findings suggest that a GABAergic pathway from the diagonal band of Broca preferentially innervates vasopressin-secreting neurosecretory supraoptic nucleus (s.o.n.) neurones, and support the view that the baroreflex-induced depression in firing of s.o.n. vasopressin-secreting neurones is mediated in large part through this input.
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PMID:A gamma-aminobutyric-acid-mediated baroreceptor input to supraoptic vasopressin neurones in the rat. 362 45

The normal cardiovascular response to hydralazine in urethane-anesthetized rats, i.e. hypotension and tachycardia, was changed to hypotension and bradycardia if the body temperature of the animals was not maintained constant by external heating, but was allowed to decrease spontaneously throughout the experiment. A similar phenomenon was observed with diazoxide. In rats maintained at a rectal temperature of 31 degrees C, hydralazine bradycardia was partially blocked by a low dose of atropine and was reversed to tachycardia by a high dose of this agent; mecamylamine failed to influence heart rate lowering in this condition. Heart rate responses in unheated animals to acetylcholine and isopropylarterenol were respectively potentiated and depressed when compared to responses in heated rats. These findings suggest that cold-induced reciprocal changes in reactivity of cardiac muscarinic and beta-adrenoceptors may be responsible for reversal of hydralazine or diazoxide tachycardia in urethane-anesthetized hypothermic rats. As a result, cardiac stimulation by the sympatho-adrenal discharge induced by hypotension is inhibited, while cardiac depression which is apparently also induced by hypotension, is facilitated. It is speculated that vasopressin, released as a consequence of the blood pressure fall, could be this negative chronotropic factor.
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PMID:Reversal by hypothermia of vasodilator-induced tachycardia in anesthetized rats. 367 83

The mechanism of the cardiodepressant effect of vasopressin was studied by measuring simultaneously myocardial contractile force and coronary blood flow (with tracer microspheres) in anaesthetized open-chest rabbits. Lysine-vasopressin administered at two dose levels (10 and 100 mu kg-1 infused in 2 min with a maintenance dose of 2 mu kg-1 min-1 between these two loading doses) to a group of 6 rabbits caused dose-dependent myocardial depression and also severely decreased coronary blood flow in a dose-dependent manner. Blood pressure remained almost unchanged but heart rate, cardiac output and total peripheral conductance were also decreased dose-dependently. In another group of 6 rabbits treated in the same way with lysine-vasopressin, darodipine (PY 108-068, 30 and 100 micrograms kg-1) was infused intravenously. It reversed the vasopressin-induced coronary constriction and cardiodepression. The high dose of vasopressin brought back cardiac depression but did not reduce coronary blood flow below baseline values. Myocardial depression could therefore not be adequately explained by the changes in coronary blood flow. In a further group of rabbits which had been subjected to cervical vagotomy and beta-adrenoceptor blockade (propranolol 1 mg kg-1 i.v.) before the experiment, vasopressin still caused coronary constriction which was reversed by darodipine, but had no effect on myocardial contractile force and heart rate. The cardiodepressant effect of vasopressin can thus be explained fully by effects on the autonomic nervous system which are reversed by lowering blood pressure, whereas the severe reduction of coronary flow did not contribute to the vasopressin-induced myocardial depression.
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PMID:Vasopressin induced myocardial depression in neurally mediated and not due to impaired coronary blood flow. 380 66

Controversy exists as to the neural network whereby peripheral arterial baroreceptor information is transmitted to vasopressin (VP)-secreting neurons of the hypothalamic supraoptic nucleus (s.o.n.). In vivo electrophysiological studies in the rat were undertaken to characterize the selective depression of VP cell activity consequent to activation of peripheral baroreceptors. Electrical stimulation of the diagonal band of Broca (DB) in the rat evoked a similar selective inhibition of vasopressinergic neurons of the s.o.n. Local application of bicuculline, a GABA antagonist, abolished both the DB-evoked and baroreceptor-induced inhibition of VP-secreting neurons. In addition, recordings from DB neurons antidromically activated from the s.o.n. displayed an increase in firing consequent to baroreceptor activation, coinciding with the suppression of firing in s.o.n. VP neurons. These observations collectively indicate that an intrinsic GABA projection arising in the DB cell group selectively inhibits vasopressinergic neurons of the s.o.n. and that this pathway mediates peripheral arterial baroreceptor activity that influences the release of VP in the neurohypophysis. These data may be of critical importance in our understanding the etiology of those forms of experimental hypertension where abnormalities in central baroreceptor pathways have been implicated but not proven.
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PMID:Neurophysiology of a central baroreceptor pathway projecting to hypothalamic vasopressin neurons. 381 62

Release of human neurophysin I (hNp I) and neurophysin II (hNp II) during insulin-induced hypoglycemia was studied in 10 unipolar depressed women before and after 4-5 weeks of standard antidepressant drug treatment with daily intravenous infusions of clomipramine. Before treatment, a significant increase of hNp I but not of hNp II serum levels in response to hypoglycemia was observed. At retest during clomipramine administration, a marked clinical amelioration occurred in all patients as determined with the Hamilton Rating Scale for Depression; the hNp I response to insulin was abolished, but no effect on hNp II concentration could be demonstrated. No correlation was found between the degree of the depression score decrease and the amplitude of the inhibition of hNp I release or serum levels of clomipramine or its metabolite, desmethylclomipramine. The meaning of this difference in reactivity of the neurohypophyseal system in the course of depressive illness, based on the pharmacological and biochemical profiles of clomipramine action, is discussed.
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PMID:Release of human neurophysin I during insulin-induced hypoglycemia in depressed patients is abolished after recovery with clomipramine treatment. 388 65

Lysine-8-vasopressin (LVP) for 10 days and in doses up to 13.5 LVP units did not significantly alter the Hamilton Depression Rating Scale scores of 12 severely depressed, treatment-resistant patients who were evaluated in a double-blind crossover study. The 24-h rhythms of melatonin, cortisol, growth hormone and prolactin appeared remarkably stable over the course of repeated measurement. LVP administration did not affect these 24-h rhythms.
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PMID:Effect of lysine vasopressin in depressed patients on mood and 24-hour rhythm of growth hormone, cortisol, melatonin and prolactin. 390 21


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