A short-term trial of an analogue of eel-calcitonin in headache.
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Adult↗
Biomedical subjects
G Clementi
Publications and source records attributed to G Clementi.
Effects of salmon calcitonin on plasma renin activity and systolic blood pressure in the rat.
Salmon calcitonin, centrally injected, increased plasma renin activity and blood pressure in rats. It is possible that the peptide through an action on the central serotonergic tone stimulated plasma renin activity with subsequent enhancement of blood pressure. Conversely, peripheral administration of the peptide increased plasma renin activity but did not cause changes in blood pressure. Probably, the enhancement of renin may be a physiological response to the renal activity of calcitonin; however, this activity does not seem to involve urinary prostaglandins.
Animals↗
[Certain central effects of calcitonin and parathormone].
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Calcitonin↗
The analgesic activity of calcitonin and the central serotonergic system.
The effect of peripherally administered cyproheptadine or reserpine and the administration of 5,7-dihydroxytryptamine (5,7-DHT) in the nucleus raphe dorsalis on the analgesic activity of salmon calcitonin (sCT) injected into the lateral ventricle were investigated in male rats. Cyproheptadine or reserpine, given respectively 30 min or 24 h before the peptide, completely abolished the analgesic activity at all the times studied. However, when reserpine was given before the peptide it increased the effect of sCT at 30 (P less than 0.01), 60 (P less than 0.001), 120 (P less than 0.01) and 180 (P less than 0.01) min. 5,7-DHT injected in the nucleus raphe dorsalis 15 days before the peptide led to complete abolition of the analgesic activity. If neurotoxin was injected 4 days before sCT, the effect of the peptide was significant (P less than 0.05) only at 60 min. The results obtained confirm that the analgesic activity of sCT may involve central serotonergic pathway(s), and that the midbrain raphe nuclei 5-HT content is an important focus for this activity.
5,7-Dihydroxytryptamine↗
Inhibition of restraint stress by systemic (Asu1,7) eel-calcitonin.
The effects of different doses of (Asu1,7) eel-calcitonin, iv injected, on gastric secretion were studied in conscious rats with pyloric occlusion. Moreover, we evaluated the activity of this analogue on gastric ulcer formation by restraint stress. It was found that 2.5 or 5 Ul/kg (Asu1,7) eel-calcitonin decreased gastric acid secretion and inhibited the development of stress-induced ulcers in rats. In the isolated rat stomach the peptide at the concentrations of 1 nM to 1 microM did not modify acetylcholine, histamine or 5-hydroxytriptamine-induced contractions. These results suggest that this peripheral activity of (Asu1,7) eel-calcitonin does not involve a direct interference with cholinergic, histaminergic or serotonergic pathways at gastric level.
Animals↗
Effect of (Asu1,7)E-CT, synthetic analogue of eel-calcitonin, on nociceptive transmission.
The effect of (Asu1,7)E-CT a deaminodicarba-analogue of the synthetic eel-calcitonin on the nociceptive transmission has been studied in mice. The analogue was intracerebroventricularly (0.0.5-0.01-0.02 U.I./kg) or intravenously (0.02-0.04-0.05 -0.1 U.I./kg) injected. This synthetic derivative of eel-calcitonin increased the antinociceptive effect also after peripheral administration. Moreover, preliminary studies on the time-course of this analogue showed that the dose of 0.1 U.I./kg i.v. injected, was able to elicit antinociceptive effect, already 5 min after the administration.
Animals↗
Hyperalgesic activity of parathyroid hormone and its fragments in male rats.
Results presented in this paper indicate that intracerebroventricular injection of parathyroid hormone reduces pain threshold in male rats. This effect is induced by whole molecule (84 amino acids) or by fragments 1-34 and 44-68 of PTH. The fragment 65-84 of PTH does not induce any change in pain threshold.
Animals↗
Role of serotonin in the analgesic activity of calcitonin.
The acute effects of peripherally administered methysergide or phentolamine on the analgesic activity of salmon calcitonin (sCT) injected into the lateral ventricle were investigated in male rats. Methysergide, but not phentolamine, significantly (P less than 0.05) antagonized the analgesic activity of sCT at 60 and 120 min after the administration of the peptide. The results obtained suggest that the analgesic activity of sCT may involve central serotonergic system(s), while the central noradrenergic system does not seem to be needed for this activity.
Analgesics↗
Prolactin and calcium metabolism: influence of hyperprolactinemia on immunoreactive parathyroid hormone levels in man and in the rat.
Serum prolactin, parathyroid hormone, P and Ca serum levels were measured in 15 patients (12 women and 3 men) with hyperprolactinemia, and in 6 normal male volunteers who underwent a TRH test (100 micrograms by rapid iv injection) in order to obtain a short-term pharmacologically-induced hyperprolactinemia. A pituitary gland graft under the kidney capsule was carried out on 26 Sprague-Dawley male rats, which became hyperprolactinemic since the transplanted pituitary was stripped of the inhibitory hypothalamic control. Another group of 10 rats was injected with L-sulpiride (0.1 mg/kg). The serum PTH levels in patients and in subjects with induced hyperprolactinemia were within the normal range and there was no correlation between serum PRL and PTH levels. The same occurred both in transplanted and L-sulpiride injected rats. Our results suggest that prolactin does not modify PTH secretion in vivo and therefore, in contrast with previous data, it should not be considered a physiologically relevant secretagogue for parathyroid hormone.
Adolescent↗
Effects of calcitonin, parathyroid hormone and its related fragments on acquisition of active avoidance behavior.
The acquisition of active avoidance response was studied in rats injected intracerebroventricularly with calcitonin (CT), parathyroid hormone (PTH) or PTH-related fragments. PTH and PTH65-84 facilitated the acquisition of shuttle-box active avoidance behavior as indicated by the number of conditioned avoidance responses and the percentage of animals reaching the learning criterion. PTH1-34 and PTH44-68, on the contrary, inhibited the acquisition of active avoidance behavior, while CT totally suppressed this behavior in the rat. It is possible that the opposite effects of PTH and CT on learning ability of the rat depend on a different action on calcium metabolism.
Animals↗
Effect of calcitonin on ACTH secretion.
We have investigated the effects of salmon calcitonin injected intracerebroventricularly on adrenocorticotropic (ACTH) secretion in rats. Salmon calcitonin was able to increase significantly (p less than 0.05) ACTH secretion at the dose of 5 ng/rat and (p less than 0.01) at the doses of 12.5, 25 and 50 ng/rat; the effect (50 ng/rat) was maximal at 30 min and still present after 60 and 120 min. The maximal dose of calcitonin produced a significant (p less than 0.05) increase in serum ACTH concentration also in stressed animals. It is suggested that calcitonin may increase serum ACTH secretion by central norepinephrine and/or 5-hydroxytryptamine pathways that regulate corticotropic releasing factor activity.
Adrenocorticotropic Hormone↗
Effects of parathyroid hormone or haloperidol-induced catalepsy and nigral GAD activity.
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Animals↗
Effects of calcitonin on the brain of aged rats.
We have recently demonstrated that calcitonin, a putative neuromodulator, may influence extrapyramidal motor system by decreasing nigro-striatal dopaminergic function. Since calcitonin is extensively used in aged patients, we have investigated whether calcitonin might influence extrapyramidal motor behavior (haloperidol-induced catalepsy and apomorphine-induced hyperactivity) in rats of different ages. Intracerebroventricular injection of salmon calcitonin (1 micrograms/kg) prevented apomorphine-induced hyperactivity in 2, 7, 18 or 21 month old rats, but potentiated haloperidol-induced catalepsy only in 2 or 7 month old rats. In addition, in all the animals salmon calcitonin significantly decreased the secretion of prolactin, an anterior pituitary hormone that may act at central level enhancing nigro-striatal dopaminergic activity.
Age Factors↗
Hypoprolactinemic action of calcitonin and the tuberoinfundibular dopaminergic system.
The effects of calcitonin on neurochemical parameters related to the tuberoinfundibular dopaminergic system have been investigated in an attempt to elucidate how calcitonin decreases serum prolactin levels. Intracerebroventricular human or salmon calcitonin injection decreases serum prolactin, medial basal hypothalamic dopamine (DA) and dihydroxyphenylacetic acid (DOPAC) and hypophysial DA and increases hypophysial DOPAC. Results suggest that calcitonin may decrease prolactin secretion via the tuberoinfundibular dopaminergic system.
3,4-Dihydroxyphenylacetic Acid↗
Effects of hyper- and hypoprolactinemia on glutamate decarboxylase activity in medial basal hypothalamus of male rat.
Haloperidol, sulpiride, domperidone and apomorphine, drugs which influence dopamine (DA) receptors and in turn prolactin (PRL) secretion have been shown to induce parallel changes in medial basal hypothalamic (MBH) glutamate decarboxylase (GAD) activity and serum PRL levels. The possibility that PRL may be involved in the effects of the drugs on MBH GAD activity is suggested in view of the evidence that hypophysectomy completely prevents drug-induced MBH GAD activity changes and that hyperprolactinemia by anterior pituitary homograft results in a significant, although small, change in the enzymatic activity.
Animals↗
[Effects of crystalloid, colloid and plasma priming on coagulation after extracorporeal circulation].
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Blood Coagulation↗
Effects of calcitonin on rat extrapyramidal motor system: behavioral and biochemical data.
The effects of i.v.c. injection of human and salmon calcitonin on biochemical and behavioral parameters related to the extrapyramidal motor system, were investigated in male rats. Calcitonin injection resulted in a potentiation of haloperidol-induced catalepsy and a partial prevention of apomorphine-induced hyperactivity. Moreover calcitonin induced a significant decrease in nigral GAD activity but no change in striatal DA and DOPAC concentration or GAD activity. The results are discussed in view of a primary action of calcitonin on the striatonigral GABAergic pathway mediating the DA-related behavioral messages of striatal origin.
3,4-Dihydroxyphenylacetic Acid↗