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Eglen, R.M., 1983. The pharmacology of calcitonin. PhD, Nottingham Trent University.
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Abstract
The antinociceptive properties of calcitonin have been studied. Antinociception was only observed after intracerebroventricular (i.c.v.) injection. There was no effect observed after i.v., i.p. or s.c. administration. The concentration of plasma calcium was reduced following administration of the hormone by all of these routes. It was concluded that antinociception induced by calcitonin was independent of its action on the concentration of plasma calcium.
The i.c.v. injection of calcium (but not magnesium) ions or the ionophore A23187, simultaneously with calcitonin antagonised the antinociceptive effects of the hormone. The i.c.v. injection of EGTA or the calcium antagonists, nifedipine and PY 108 068, simultaneously with calcitonin, potentiated the antinociceptive effects of calcitonin. Similar results have been reported for the opiates. However, the opiate antagonist, naloxone, was relatively ineffective in reversing the antinociceptive effects of the hormone.
Withdrawal of animals from chronic pretreatment with calcitonin administered by s.c. injection, produced a long lasting hyperalgesia. In these animals, the antinociceptive effects of calcitonin, but not aspirin, were reduced.
In contrast to that of the opiates, calcitonin was not effective in altering the total calcium concentration of the brain, after i.c.v. or s.c. injection. However, in a similar fashion to the opiates, calcitonin reduced the uptake of 45 calcium by stimulated and non-stimulated brain slices, in vitro.
Calcitonin was ineffective when applied to the superfused rat colon, in vitro. This tissue produced a contractile response to the opiates. Calcitonin, unlike the opiates, did not reduce the blood pressure of the anaesthetised normotensive rat. However, it did resemble the action of naloxone, in producing a pressor effect in rats rendered hypotensive by haemorrhage.
In contrast to previous workers, calcitonin was found to be ineffective in increasing the activity of cortical acetylcholinesterase.
It is concluded that antinociception induced by calcitonin resembles that of the opiates, in that an alteration in calcium flux is involved. However, the hormone is unlikely to act via the opiate receptor to produce this response.
| Item Type: | Thesis | ||||
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| Creators: | Eglen, R.M. | ||||
| Date: | 1983 | ||||
| ISBN: | 9781369315950 | ||||
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| Divisions: | Schools > School of Science and Technology | ||||
| Record created by: | Linda Sullivan | ||||
| Date Added: | 22 Sep 2020 15:02 | ||||
| Last Modified: | 16 Aug 2023 10:45 | ||||
| URI: | https://irep.ntu.ac.uk/id/eprint/40887 |
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