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)

Stimulation of the sympathetic outflow (spinal cord segments T 7-9) in pithed rats resulted in an increase in mean arterial pressure, heart rate, total peripheral vascular resistance and cardiac output. The increase in blood pressure and peripheral resistance was markedly depressed by prazosin and to a lesser extent by yohimbine, suggesting that these responses were mediated primarily by postjunctional alpha 1-adrenoceptors. The calcium entry blockers nifedipine, tiapamil and verapamil also depressed pressor responses and the increase in total peripheral resistance to electrical stimulation of the sympathetic outflow in these rats. This depression resulted primarily from an effect on peripheral vascular resistance components, as cardiac output remained unaffected by the calcium entry blockers. This conclusion was supported by studies on isolated, perfused rat renal arteries. Vasoconstrictor responses of this in vitro preparation to perivascular nerve stimulation were depressed by 1,000-fold lower concentrations of prazosin than rauwolscine, demonstrating the predominantly alpha 1-adrenoceptor nature of these effects. Likewise, these vasoconstrictor responses were depressed by nifedipine, tiapamil and verapamil in a concentration-dependent manner. The results of this study suggest that vasoconstrictor responses of rat resistance vessels to sympathetic nerve stimulation are mediated primarily by postjunctional alpha 1-adrenoceptors and can be inhibited by calcium entry blockers. This implies that contractile responses of these resistance vessels to alpha 1-adrenoceptor stimulation are not independent of the availability of extracellular calcium.
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PMID:Calcium entry blockers inhibit vasoconstrictor responses to sympathetic nerve stimulation mediated by alpha 1-adrenoceptors. 299 40

Aminophylline reduces hypoxic ventilatory depression in newborn piglets and can enhance the release of catecholamines (CATs), which in turn may stimulate ventilation. To determine if the effect of aminophylline on ventilation was due to the release of CATs, we measured plasma CATs and ventilation in two groups of spontaneously breathing newborn piglets less than 4 days old, treated with either aminophylline (n = 7) or normal saline solution (n = 6) during both normoxia and hypoxia. The piglets were anesthetized with ketamine and xylazine and intubated, and the femoral artery was catheterized. Epinephrine and norepinephrine were measured before and 30 minutes after treatment with aminophylline (15 mg/kg) or normal saline. The animals were exposed to 10% oxygen and the CATs again measured after 5 minutes of hypoxia. Respiratory rate, expiratory flow integrated to minute ventilation (VE), heart rate, and blood pressure were continuously recorded. CATs were assayed by high-pressure liquid chromatography with electrochemical detection. Treatment with aminophylline during normoxia was associated with an increase in tidal volume. During hypoxia, treatment with aminophylline prevented a fall in VE and respiratory rate seen in the normal saline group. Epinephrine and norepinephrine increased during hypoxia, but there was no difference between the groups at 5 minutes. In our model the increase in CATs observed during hypoxia was not enhanced by aminophylline. This is consistent with the hypothesis that some mechanism other than catecholamine release is responsible for the effect of aminophylline in reducing neonatal hypoxic respiratory depression.
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PMID:Aminophylline reduces hypoxic ventilatory depression without increasing catecholamines. 309 64

Acute exposure of rainbow trout (Salmo gairdneri) to low external calcium (25 microM) caused an immediate but transient increase in plasma epinephrine concentration that may have been related to a concomitant depression of blood pH. Intra-arterial infusion of epinephrine at normal ambient calcium levels (0.35 mM) for 4 h caused circulating levels of epinephrine to rise from 2.9 X 10(-9) to 8.0 X 10(-8) M but did not affect norepinephrine levels, or branchial unidirectional calcium fluxes. Active (ATP-dependent) calcium transport across basolateral plasma membranes prepared from gill epithelial cells was not affected by pretreatment of fish with epinephrine or by direct application of epinephrine or cAMP, in vitro. Epinephrine infusion elevated urine flow rate, decreased urine pH, and increased urine phosphate levels significantly. Net renal calcium efflux increased significantly as a result of the increased urine flow rate. It is concluded that epinephrine does not stimulate branchial calcium uptake or renal conservation of calcium in rainbow trout at normal external calcium levels and therefore we cautiously suggest that epinephrine is unlikely to be involved in calcium balance during periods of exposure to low external calcium. Instead, epinephrine may play a role in compensating the acid-base disturbances and the increased branchial water influx that are associated with exposure to low ambient calcium.
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PMID:Effects of epinephrine on branchial and renal calcium handling in the rainbow trout. 338 70

In the liver of adjuvant arthritic rats perfused with a hemoglobin-free buffer solution, the rate of metabolism of a model drug, 2,6-dichloro-4-nitroanisole, was approximately half that of the control, while the bile flow rate was normal. Granulation tissue extracts and arthritic rat serum had no effect on the activity of CNA metabolism in normal rat liver preparations. In the perfused normal rat liver, the rate of CNA metabolism was inhibited by addition of prostaglandin (PG) E1, PGE2, and PGF2 alpha, respectively, in a final concentration of 0.5 microM. The inhibition by PGE1 was increased in the concentration range from 0.1 to 2.5 microM. The bile flow rate was not affected by the added PGs. However, these PGs had no direct effect on the CNA demethylating activity of the isolated hepatocytes from normal rat liver in a high concentration of 10 microM. Serotonin stimulated slightly CNA metabolism and bile production in the perfused livers by the intermittent infusion, but was without effect in the isolated hepatocytes. Epinephrine and histamine had no significant effect on CNA metabolism in both liver preparations. A similar pattern of the inhibition of CNA metabolism by PGs was reproduced in the normal rat liver perfused with the medium containing the supernatant of the hepatic nonparenchymal cells incubated in the presence of PGE1. The involvement of liver sinusoidal cells as secretory cells in depression of hepatic drug metabolism has been discussed.
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PMID:Prostaglandins: a possible mediator to inhibit hepatic drug metabolism in adjuvant arthritic rats. 346 29

This study was performed on chloralosed rats in order to examine the influence of a minor blood loss on duodenal HCO3- secretion. The HCO3- output was measured by in situ titration in a duodenal segment. Blood loss of 0.3 ml per 100 g body wt (approximately 5% of total blood volume) and 0.6 ml per 100 g body wt (approximately 10% of total body volume) reduced duodenal HCO3- secretion by about 18 and 31%, respectively. Adrenal ligation increased basal output of HCO3- but did not affect the bleeding-induced response. Thoracic epidural anaesthesia or splanchnicotomy did not affect the basal secretion but markedly reduced the depression of duodenal HCO3- secretion due to blood loss. Vagotomy lowered basal duodenal HCO3- secretion and blood loss did not reduce alkaline output in these animals. However, electric stimulation of the cut vagal nerves raised the duodenal HCO3- secretion to a similar level as in rats with intact vagal nerves. In this group blood loss reduced the duodenal HCO3- output as in rats with intact nerves. It is suggested that a small blood loss, via an activation of the sympathetic nervous system, reduces the vagally controlled part of the duodenal HCO3- secretion and that this effect is conveyed in the splanchnic nerves.
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PMID:Bleeding inhibits vagally induced duodenal HCO3- secretion via activation of the splanchnic nerves in anaesthetized rats. 360 15

Adrenal weight was significantly higher in 16 victims of violent suicide than in 10 subjects who died suddenly from other causes. Since approximately half of suicide victims are depressed, these results support an association between depression and hypertrophy of the adrenal cortex.
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PMID:Increased adrenal weight in victims of violent suicide. 363 21

Stress is believed to increase hematocrit. Groups of patients with generalized anxiety disorders and normal volunteers matched on age and sex were compared on resting levels of state anxiety, trait anxiety, depression, pulse rate, blood pressure and hematocrit. There were no differences between the patients and controls on hematocrit, although the former showed significantly higher state anxiety, trait anxiety and depression. The measurements were repeated in the anxious patients after one-half of the subjects received an intravenous infusion of epinephrine and the other half saline. Epinephrine was associated with significant increases in state anxiety, pulse and systolic blood pressure, but not with any hematocrit or plasma volume changes.
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PMID:Hematocrit and anxiety. 373 74

Adenylate cyclase activity of the washed particles from the ventricles of rats made hypothyroid by propylthiouracil (P.T.U.) treatment was studied in the absence or presence of different concentrations of catecholamines, guanylimido-diphosphate (GppNHp) and NaF. The washed particles preparation of hypothyroid rat displayed higher basal adenylate cyclase activity in comparison to that in the euthyroid animal. Fluoride stimulation was unaltered but GppNHp stimulation was markedly depressed over a wide range of concentrations in the hypothyroid heart washed particles. Epinephrine stimulation in the presence of GppNHp was altered only at 10(-5) to 10(-4)M concentrations. Depressed responsiveness of cardiac adenylate cyclase to GppNHp and epinephrine was also found in washed particles of thyroidectomized rats. Depression of GppNHp or epinephrine response in hypothyroid animals was reversed 48 hours after T3 administration. In contrast to the washed particulate preparation, no depressions in the responses of adenylate cyclase to GppNHp or epinephrine were seen in the purified sarcolemmal membranes from P.T.U. induced hypothyroid or thyroidectomized rat hearts. It is proposed that altered guanine nucleotide binding or altered guanine nucleotide binding protein-catalytic subunit interaction in the adenylate cyclase system may be an underlying mechanism of depressed positive inotropic action of catecholamines in the hypothyroid state.
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PMID:Alterations in the cardiac adenylate cyclase activity in hypothyroid rat. 385 Jul 75

1. Noradrenaline and adrenaline reduce the output of acetylcholine by the guinea-pig ileum longitudinal strip by up to 80%, both in resting conditions and after stimulation. The effect is graded with dose, and is detectable with noradrenaline 2 x 10(-7) g/ml. Adrenaline is approximately 4 times as active as noradrenaline, and its action after being washed out is more persistent.2. If resting output is high, both amines have a proportionately greater effect and their action, as dosage is increased, is to reduce resting output to a basal level, relatively constant from strip to strip, of about 10 ng/g/min.3. With stimulation, the effect of the amine is greater at low frequencies, when the output per volley is high, than at high frequencies. The effect is reduced by increasing the number of shocks delivered. There thus appears to be a basal output per volley, of the order of 1-2 ng/g/volley, which can be reached either by relatively rapid stimulation, by prolonged stimulation, or by treatment with these amines.4. If noradrenaline is applied during continued stimulation at 40/min, the depression of acetylcholine output during its presence is followed by an augmented output when the drug is withdrawn. The magnitude of this "overshoot" increases with the duration of noradrenaline exposure.5. Phenylephrine 4 mug/ml. and amphetamine 20 mug/ml. reduced the acetylcholine output, but isoprenaline 1 mug/ml., dopamine 1 mug/ml. and methoxamine 10 mug/ml. were ineffective.6. Phenoxybenzamine reduced the resting output and increased the stimulation output. Of the two other blocking agents examined, phentolamine had no effect on either resting or stimulation output and ergotamine transiently reduced stimulation output. The effect of phenoxybenzamine was not due to a reaction with either adrenoceptive or muscarinic receptors.7. Phenoxybenzamine, phentolamine and ergotamine abolished the effect of adrenaline and noradrenaline on both resting output and on output in response to stimulation.8. In strips obtained from animals treated with reserpine and guanethidine, a rise in resting acetylcholine output and in stimulation output at low frequencies was found. In these conditions, noradrenaline was still effective.9. Reducing the hydroxytryptamine content of the strips by treatment with p-chloro-(+/-)-phenylalanine did not significantly affect acetylcholine output.10. It is concluded that acetylcholine output by the nervous networks of the longitudinal strip is under the normal control of the sympathetic by a species of presynaptic inhibition mediated by alpha receptors. This implies that for a tissue under dual autonomic control, withdrawal of sympathetic control will lead to a parasympathetic response which is not only unopposed but also itself enhanced.
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PMID:The inhibitory action of noradrenaline and adrenaline on acetylcholine output by guinea-pig ileum longitudinal muscle strip. 430 25

1. The guinea-pig seminal vesicle has been shown to be a very suitable test object for the study of mechanisms involving alpha-adrenoceptive receptors, because no beta-receptors were found in this preparation.2. Adrenaline, noradrenaline and phenylephrine were directly acting agonists, their ED50 values being 7.1 x 10(-6)M, 1.5 x 10(-5)M and 2.7 x 10(-5)M, respectively.3. Pretreatment with reserpine had no influence on the contractions caused by adrenaline, noradrenaline and phenylephrine but abolished or greatly reduced the contractions caused by dopamine. Cocaine enhanced the effects of adrenaline, noradrenaline and phenylephrine and reduced those of dopamine.4. Pronethalol (6.8 x 10(-5)M) reversed the alpha-receptor blockade by dibenamine, ergotamine and phentolamine of responses to adrenaline, noradrenaline and phenylephrine; it did not affect the blockade by dibenamine of responses to histamine.5. Reversal of the blockade by dibenamine was observed only when its concentration was such that it caused a parallel shift of the dose-effect curves of the agonists to the right; higher concentrations, which caused an unsurmountable depression of the maximal contraction, were not antagonized by pronethalol.6. It is assumed that the reversal is dependent on a direct action on alpha-receptors, "spare receptors" being probably involved.
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PMID:Reversal by pronethalol of dibenamine blockade: a study on the seminal vesicle of the guinea-pig. 438 84


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