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)

Thirteen patients with painful Paget's disease of bone were treated as outpatients with low doses of synthetic salmon calcitonin 22.5-50 mug three times weekly. Treatment produced full remission of pain in a mean time of 5.5 weeks and a mean depression of serum alkaline phosphatase activity of 33%.The interval before symptomatic relief could not be predicted from the variables studied. The ultimate fall in serum alkaline phosphatase activity, however, could be predicted from the initial levels and from the early rate of decrease (P < 0.001). Biochemical resistance to treatment, which occurred in three cases, could be related to the dose and duration of treatment.Prolonged remissions of pain may occur which are not related to biochemical remission, to the dose of calcitonin, or to the duration of treatment. The side effects attributable to salmon calcitonin were transient nausea (in nine patients), transient flushing (in four), diarrhoea (in two), and rash (in one) though in only one patient did treatment have to be withdrawn prematurely because of these effects.
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PMID:Treatment of Paget's disease of bone with synthetic salmon calcitonin. 447 16

After having reviewed the properties of calcitonin (Ct), a hormone involved in calcium-phosphate metabolism and bone turnover, mention is made of the effects of Ct at the level of the CNS and its role as a neuromediator interfering with endorphins, prolactin, dopamine and the Ca concentration of the CSF. Overall's rating scale was used to evaluate the effects of synthetic salmon Ct in nine subjects with severe depression syndromes refractory to normal therapy. The study demonstrated statistically significant improvements of the major symptoms (behavioural excitation, depression, agitation, anxiety and affectivity). The favourable results justify broader and more detailed studies involving the relationship between Ct and psychopathology.
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PMID:A preliminary study on the use of calcitonin in clinical psychopathology. 614 Nov 15

Parathyroid hormone (PTH) and calcitonin exert well known effects on the renal tubule which are thought to involve specific hormone receptors and adenyl cyclase. In the intestine, it is not clear whether the action of PTH and calcitonin is only indirect or also direct, and their mechanisms of action are much less well established. In the present study, possible direct effects of PTH and calcitonin on Na+ transport in isolated intestinal epithelial cells of rats were investigated. In the presence of bovine PTH (1.2 I.U/ml) in the incubation medium, the Na+ efflux rate constant (oKNa) of isolated enterocytes was significantly reduced when compared to that in control experiments with the hormone vehicle only. The mean depression of oKNa induced by bovine PTH was 26% as compared to the control (100%) and to that induced by ouabain (4.0 mM) which was 44%. No depressant effect of bovine PTH on oKNa was observed when the isolated enterocytes were incubated with ouabain (4.0 mM). Thus, bovine PTH appeared to inhibit the ouabain-sensitive Na+ pump. When incubating the isolated epithelial cells in an EGTA-containing CA2+-free medium, bovine PTH lost its capacity to inhibit oKNa. Thus, the presence of extracellular Ca2+ appeared necessary for the inhibitory effect of bovine PTH. In contrast to its effect on oKNa, bovine PTH induced no change in net Na+ uptake by isolated enterocytes. Moreover, no significant effect on enterocyte Na+ transport could be demonstrated for salmon or porcine calcitonin at two different concentrations in the incubation medium, Neither bovine PTH nor salmon calcitonin induced significant changes in enterocyte cyclic AMP or cycle GMP concentrations. It was concluded that bovine PTH, but not calcitonin, exerted a directed inhibitory effect on the ouabain-sensitive oKNa of isolated rat enterocytes. The effect of bovine PTH occurred without measurable activation of the cyclic nucleotide system but needed the presence of Ca2+ in the incubation medium to be operative.
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PMID:Rat enterocyte Na+ transport in vitro. Action of parathyroid hormone and calcitonin. 627 49

Goldfish showed a significant reduction in their plasma sodium and calcium levels 1 h after receiving 50 i.u. calcitonin per kg body weight. When 100 i.u. calcitonin were injected there was a significant fall in circulating levels of both sodium and calcium and also of chloride ions compared with those found in untreated control animals. Administration of calcitonin to immature eels adapted to either freshwater or seawater conditions showed no significant change in plasma ion composition at doses of 10 i.u. per kg body weight or less. However, doses of 50 and 100 i.u. caused significant reductions in plasma sodium, chloride and calcium ion levels compared with sham-injected control animals. When immature eels were given 100 i.u. calcitonin per kg body weight there were significant reductions in the plasma levels of sodium, chloride and calcium ions but the timing of these changes was slightly different. In freshwater-adapted eels, the depression of plasma sodium was seen after 30 min and lasted for up to 2 h, whilst depression of plasma chloride and calcium was not seen until 1 h after injection. In addition, whilst the lowering of plasma chloride ions lasted up to 2 h after injection, the plasma calcium had returned to the preinjection control level by this time. In seawater-adapted eels the depression of sodium, chloride and calcium levels was seen at 30 min and the effect continued for up to 2 h after injection when the depression was no longer apparent.
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PMID:Depression of sodium, chloride and calcium ions in the plasma of goldfish (Carassius auratus) and immature freshwater- and seawater-adapted eels (Anguilla anguilla L.) after acute administration of salmon calcitonin. 687 32

It was examined whether calcitonin (CT)-induced hypocalcemia could modify the pharmacological actions of kanamycin sulfate (KM). CT produced a dose dependent and long-lasting hypocalcemia in urethane anesthetized and conscious rats. In anesthetized rats, KM infusion depressed the indirectly elicited contractions of the tibialis anterior muscle (MC), mean arterial pressure (AP), heart rate (HR) and respiratory rate. CT did not influence the stability of the above parameters and slightly modified the neuromuscular depression of KM. In conscious rats, KM infusion produced spontaneous and complete head drop, loss of corneal reflex, respiratory arrest and also depressed AP and HR. Much higher doses of KM were required to induce the same pharmacological actions in conscious than in anesthetized rats. CT dose-dependently potentiated the pharmacological actions of KM. A highly significant linear correlation between the serum total calcium levels and the KM dose inducing spontaneous head drop was observed. These data indicate that, in conscious rats, the actions of KM are dependent on the serum calcium levels. In the same experimental conditions, neither CT-induced hypocalcemia nor anesthesia did modify significantly the pharmacological actions of d-tubocurarine.
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PMID:Effects of calcitonin-induced hypocalcemia on the neuromuscular and cardiovascular depressive actions of kanamycin in anesthetized and conscious rats. 722 26

Permanent hypocalcemia complicating thyroidectomy is a rare complication, whereas transient post-thyroidectomy hypocalcemia occurs frequently. Ten patients were studied in an attempt to elucidate the underlying mechanisms. An early and transient postoperative rise in calcitonin (CT) corresponding to a decline in calcium levels was demonstrated. Though there was no significant depression of parathyroid hormone (PTH) levels, the failure of the parathyroids to respond to hypocalcemic stimuli suggests a degree of at least transient parathyroid insufficiency. Transiently elevated CT levels appear to play a significant role in the commonly observed early, transient post-thyroidectomy hypocalcemia following subtotal and total thyroidectomy.
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PMID:The role of calcitonin and parathyroid hormone in the pathogenesis of post-thyroidectomy hypocalcemia. 723 Nov 95

We examined the role of calcitonin gene-related peptide (CGRP) in cortical spreading depression (CSD)-induced dilation of rabbit pial arterioles. In urethan-anesthetized rabbits instrumented with a closed cranial window, CSD induction with KCl dilated pial arterioles from 86 +/- 10 to 132 +/- 13 (mean +/- SE, n = 6) microns (a 54 +/- 9% increase). Topical administration of 12.8 microM CGRP-(8-37), a competitive inhibitor of the CGRP receptor, reduced CSD-induced pial dilation from 54 +/- 9% baseline to 33 +/- 9% (P < 0.05). Removal of the receptor antagonist from the brain surface restored CSD-induced dilation to 59 +/- 11% (P < 0.05, compared with the response with the antagonist present). In other animals, we showed that this dose of the CGRP antagonist attenuated arteriolar dilation to topically applied 10(-7) M CGRP (n = 5), but it did not alter arteriolar dilation to arterial hypercapnia. We also evaluated the dilator potency of substance P (SP) compared with CGRP. Dilation with 10(-7) M SP was only 22 +/- 11%, whereas arterioles dilated to 57 +/- 7% above baseline diameter with 10(-7) M CGRP. We conclude that CGRP contributes to the transient arteriolar dilation that is characteristic of CSD.
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PMID:Calcitonin gene-related peptide promotes cerebrovascular dilation during cortical spreading depression in rabbits. 751 95

To determine the role that vasoactive neuropeptides, calcitonin gene-related peptide, and substance P play in tissue-blood flow regulation during early septic shock, we examined the responsiveness of arteries removed from pigs 3 h after administration of Escherichia coli lipopolysaccharide or saline vehicle. The carotid, cranial mesenteric, and left anterior descending coronary arteries were excised, and rings were cut from each vessel. Constrictor responses were obtained to cumulative doses of norepinephrine or potassium chloride. Rings were reconstricted and challenged with acetylcholine, substance P, calcitonin gene-related peptide, and nitroglycerin. Lipopolysaccharide significantly increased the cranial mesenteric artery's response to high concentrations of norepinephrine and the response to nitroglycerin in all vessels. This enhancement of responses to nitroglycerin suggests augmented smooth-muscle responsiveness to an exogenous source of nitric oxide, possibly associated with early depression of basal endothelial function. Depression of agonist-induced nitric oxide release may mask such enhancement with endothelial-dependent dilators and may enhance the response to adrenergic constrictors in some vascular beds.
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PMID:Early endotoxic shock results in enhanced vasodilator responses to nitroglycerin but unaltered responses to neuropeptides calcitonin gene-related peptide and substance P. 753 18

1. The ability of capsazepine, a recently developed capsaicin receptor antagonist, to prevent the effects of capsaicin on the rat isolated urinary bladder (contraction) and vas deferens (inhibition of electrically-evoked twitches) was compared to that of ruthenium red, a dye which behaves as a functional antagonist of capsaicin. 2. In the rat bladder, capsazepine (3-30 microM) produced a concentration-dependent rightward shift of the curve to capsaicin without any significant depression of the maximal response to the agonist. By contrast, ruthenium red (10-30 microM) produced a non-competitive type of antagonism, characterized by marked depression of the maximal response attainable. Similar findings were obtained in the rat isolated vas deferens in which capsazepine (10 microM) produced a rightward shift of the curve to capsaicin while ruthenium red (3 microM) depressed the maximal response to the agonist. 3. At the concentrations used to block the effect of capsaicin, neither capsazepine nor ruthenium red affected the contractile response of the rat urinary bladder produced by either neurokinin A or electrical field stimulation or the twitch inhibition produced by rat alpha-calcitonin gene-related peptide (alpha CGRP) in the vas deferens. 4. These findings provide additional evidence that both capsazepine and ruthenium red are valuable tools for exploration of the function of capsaicin-sensitive primary afferent neurones. The antagonism of the action of capsaicin by capsazepine is entirely consistent with the proposed interaction of this substance with a vanilloid receptor located on primary afferents, while the action of ruthenium red apparently involves a more complex, non-competitive antagonism.
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PMID:A comparison of capsazepine and ruthenium red as capsaicin antagonists in the rat isolated urinary bladder and vas deferens. 768 39

Neither the novel peptide, islet amyloid polypeptide (IAPP), nor its homologue, calcitonin gene-related peptide (CGRP), contracted guinea pig isolated trachea (GPT), but on preparations contracted with KCl (40 mM), both caused concentration-related relaxation (1 nM-3 microM). Relaxant curves to both were shallow and slow in development, with clear maxima not being obtained. The protease inhibitors, phosphoramidon (1 microM), leupeptin (50 microM), bestatin (100 microM), soya bean trypsin inhibitor (1 microM), and aprotinin (5 microM), together had no effect on relaxations to CGRP, but depressed those to IAPP. Aprotinin appeared to be responsible for this depression. The specific CGRP antagonist, CGRP(8-37), 1-10 microM, had no effect on relaxations to either peptide. These findings demonstrate that IAPP relaxes GPT in a similar manner to CGRP.
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PMID:The effects of IAPP and CGRP on guinea pig tracheal smooth muscle in vitro. 785 76


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