Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A series of [(epsilon-aminoalkanoyl)amino]-6,11- dihydrodibenzo[b,e]thiepins and -5H-dibenzo[a,d]cycloheptenes and related compounds were synthesized and evaluated for calcium antagonistic activity by calcium-induced constriction of potassium-depolarized rat aorta. Semiempirical molecular orbital calculations of the dibenzotricyclic systems indicated that calcium antagonistic activity increased with a decrease of the angle between the planes of the two phenyl rings. AM1 net charge calculations showed that a neutral or positive charge distribution in the bridge portion was necessary for activity. 11-[[4-[4-(4-Fluorophenyl)-1- piperazinyl]butyryl]amino]-6,11-dihydrodibenzo[b,e]thiepin maleate (16, AJ-2615) showed a more gradual and longer lasting antihypertensive effect than diltiazem and nifedipine in spontaneously hypertensive rats (SHR) administered orally. Compound 16 also possessed antianginal effects in methacholine-induced ST elevation and vasopressin-induced ST depression tests in rats. The alteration of the dibenzotricyclic system of 16 to 5H-dibenzo[a,d]cycloheptene (19, 5-[[4-[4-(4-fluorophenyl)-1-piperazinyl]-butyryl]amino]-5H- dibenzo[a,d]cycloheptene) resulted in selectivity for cardiac tissue over vascular tissue, thereby conferring antianginal activity without an effect on blood pressure. Antianginal potencies of 16 and 19 were equal to or somewhat more potent than those of diltiazem.
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PMID:A new class of calcium antagonists. 2. Synthesis and biological activity of 11-[[4-[4-(4-fluorophenyl)-1-piperazinyl]butyryl]amino]-6,11- dihydrodibenzo[b,e]-thiepin maleate and related compounds. 200 73

The hypothesis that the release of vasopressin-associated neurophysin (hNpI) or oxytocin-associated neurophysin (hNpII) is modified by a course of electroconvulsive therapy (ECT) was tested by the measurement of serum neurophysins before and after the first and last ECTs given to 17 unipolar depressed patients. Neither basal nor ECT-induced neurophysin release changed between the first and last ECTs. Data from the present study were combined with data from a previous published study to provide a sample of 29 unipolar depressed patients. In this extended sample, the release of hNpII after the first ECT was significantly correlated with improvement in symptoms of depression over a course of ECT as measured by the Hamilton Rating Scale for Depression and the Montgomery-Asberg Depression Rating Scale.
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PMID:Improvement in depressive illness is not associated with altered release of neurophysins over a course of ECT. 201 24

Neurophysins are neuropeptides (MW +/- 10,000) synthetized together with active nonapeptides vasopressin (AVP) and oxytocin (OT). The original description of the radioimmunoassay for neurophysins in 1969 allowed us to demonstrate the concomitant, equimolecular, release of them together with AVP and OT, thus bringing strong arguments in favour of neurohypophyseal exocytosis. Beside the use of those RIAs as direct indexes of neurohypophyseal release in various physiological and pathological conditions, we have been interested these last two years, to the putative use of neurophysins RIA as direct neuroendocrine markers in various neuropsychiatric diseases (depression, mania, schizophrenia) and paraneoplastic syndromes (SIADH).
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PMID:[Neurophysins]. 209 28

Patients with end stage renal failure have been shown to have higher basal concentrations of plasma arginine vasopressin than subjects with normal renal function. Immunoreactive vasopressin was detected in plasma from patients with severe chronic renal failure and a healthy subject at an elution volume identical to that previously determined with synthetic vasopressin. Assay of all fractions yielded identical chromatograms in the renal failure and healthy control groups. We conclude that the plasma immunoreactive vasopressin in end stage renal failure plasma coelutes with synthetic vasopressin and that the elevated concentrations found in these patients are not due to non-specific depression of binding in the vasopressin radioimmunoassay by circulating substances in renal failure.
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PMID:Immunoreactive vasopressin in end stage renal failure. 225 98

There is evidence for an involvement of the hypothalamic paraventricular nuclei (PVN) in the regulation of pineal melatonin synthesis in rats. Since electrical stimulation of the PVN or the systemic administration of arginine-vasopressin (AVP) result in a depression of the nocturnal melatonin surge, this neuropeptide appears to be pivotal for the transduction of PVN-efferent, pinealopetal signals. We therefore used an AVP-deficient animal model, the Brattleboro rat, to further investigate the mechanisms responsible for pineal regulation. Anesthetized adult male animals received 2 min of bilateral electrical stimulation of the PVN either during the day or at night. Thirty min later, pineal glands were removed and pineal N-acetyltransferase (NAT) activities and melatonin contents were determined. Stimulation resulted neither during the day nor at night in any significant alterations of pineal NAT activity or melatonin content when compared to control or sham-stimulated animals. These data further support the proposed modulatory role of AVP for the regulation of melatonin synthesis in the Epiphysis cerebri of genetically intact rats.
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PMID:The role of the hypothalamic paraventricular nuclei for the regulation of pineal melatonin synthesis: new aspects derived from the vasopressin-deficient Brattleboro rat. 231 35

A decreased secretion of arginine vasopressin (AVP) has been implicated in depression. In order to further investigate this hypothesis, we studied the plasma level of the specific peptidergic carrier of AVP, vasopressin neurophysin (hNpI), in 26 depressed inpatients and 16 matched normal controls. On the other hand, AVP has also been involved in the pathophysiology of the cortisol postdexamethasone nonsuppression frequently observed in depression. Therefore, we investigated concomitantly hNpI and cortisol during a dexamethasone (DXM) suppression test. hNpI and cortisol were assessed by radioimmunoassay at 8 AM and 8 PM during 4 consecutive days. From days 2 to 3, 4 mg (DXM) was given orally. hNpI values were not affected by DXM administration. Compared with controls, patients showed higher pre- and post-DXM cortisol values and lower hNpI values. No difference in hNpI values was observed between DXM escapers or nonescapers. Our results are consistent with an impaired AVP secretion in depression and fail to support a role of AVP in the early cortisol escape.
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PMID:Plasmatic vasopressin neurophysin in depression: basic levels and relations with HPA axis. 235 30

The anterodorsal part of the third ventricle of conscious ducks was perfused intracerebroventricularly (icv) for 10 min with norepinephrine (NE) or with its agonists phenylephrine (alpha 1, Phe), isoproterenol (beta, Iso), and clonidine (alpha 2, Clo) in artificial CSF (aCSF). Their effects on the plasma level of antidiuretic hormone (AVT, arginine vasotocin in birds), urine excretion, heart rate (HR), and mean arterial pressure (MAP) were investigated in steady-state water diuresis. The correct position of the icv cannula was confirmed by enhanced AVT release and antidiuresis in response to icv perfusion of aCSF made hypertonic (400 mosmol/kgH2O) by adding NaCl. Icv perfusion with hypertonic aCSF and 750 ng/min NE had comparable effects on AVT release and urine excretion, but hypertonic aCSF caused small increases in MAP and HR, whereas NE depressed both MAP and HR. Antidiuresis and circulatory depression caused by NE icv perfusion was dose dependent. Among the adrenergic agonists perfused at similar doses (188 ng/min), only Iso stimulated AVT release. Iso and Phe had small depressive effects on MAP and HR (less than 10%). Clo depressed circulation by greater than 20% for longer than 60 min, and AVT release became significantly reduced 30 min after the start of icv perfusion. The consistent results in ducks contrast with the equivocal data hitherto reported for central stimulations with NE or its agonists in mammals and may be due to the concentric perfusion system used in our study for localized stimulations in the vicinity of the paraventricular nucleus.
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PMID:ADH, renal, and circulatory responses to adrenergic stimulation in anterior third ventricle. 238 40

Vasopressin may be involved in normal memory functions and may alleviate certain memory impairments. In this study, the usefulness of vasopressin to relieve electroconvulsive therapy (ECT)-induced memory impairment was evaluated using a placebo-controlled, random assignment, double-blind design. Patients were 33 depressives receiving bilateral ECT. Vasopressin, in a nasal spray, was administered q.i.d. from the first through the fifth ECT. Extensive memory testing evaluated both retrograde and anterograde amnesia; ratings of depression and patient ratings of subjective memory complaints were also obtained. Results did not show statistically significant evidence of benefit from vasopressin, though a number of comparisons were in the predicted direction. The role of vasopressin in reducing memory impairment of various types remains to be elucidated.
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PMID:A placebo-controlled evaluation of vasopressin for ECT-induced memory impairment. 240 15

The effect of antihypertensive drugs on receptor-dependent increase in Ca2+ basal level and its changes under stimulators action (thrombocytes activating factor, ADP and vasopressin) were studied by means of a fluorescent calcium probe "quin-2". Nifedipine blocked receptor-dependent increase of Ca2+ in thrombocytes in vitro as well as by oral administration, which was accompanied by decrease in vascular tone and BP. The degree of BP decrease correlated with that of depression of receptor-dependent increase of Ca2+ in thrombocytes. Combined therapy including nifedipine, propranolol and a diuretic resulted in more manifest inhibition of receptor-dependent calcium channels than monotherapy with nifedipine. Effect of antihypertensive drugs evidently depends on their influence on receptor-dependent Ca2+ cellular entrance.
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PMID:[Effect of hypotensive therapy on a receptor-dependent increase in Ca2+ in the thrombocytes of patients with hypertension]. 245 72

The interaction of the benzothiazolamine R 56865 with the nifedipine-sensitive component of the serotonin (5-HT)-, angiotensin II (AII)- and arginine-vasopressin (AVP)-induced contractions was studied in the isolated rat aorta. Nifedipine caused concentration-dependently (10(-9)-10(-6) mol/l) a slight rightward shift accompanied by a limited depression of the maximum of the concentration-response curves for 5-HT-, AII- and AVP-induced contractions. R 56865 (10(-5) mol/l) antagonized the contraction elicited by 5-HT and AII in a similar manner as nifedipine. The effect of R 56865 on 5-HT- and AII-induced contractions was no longer observed after pretreatment with nifedipine. The AVP-induced contraction was not affected by R 56865 (10(-5) mol/l). As shown previously, R 56865 is a weak inhibitor of potential-operated channels but inactive on Ca2+ channels activated by NA. In conclusion, R 56865 does not only differentiate between depolarization and receptor-stimulation, but also between the activation of Ca2+ channels by different types of receptors. We propose that R 56865 may interact with Ca2+ channels at a site which plays a role in their activation.
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PMID:R 56865 differentiates between contractile agents with respect to the nifedipine-sensitive component in the isolated rat aorta. 255 25


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