Use this URL to cite or link to this record in EThOS: https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.796056
Title: Factors affecting the release of transmitters in the heart
Author: Boyle, Stephen J.
Awarding Body: University of Glasgow
Current Institution: University of Glasgow
Date of Award: 1988
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Abstract:
1. The aim of this study was to investigate the presynaptic interactions that exist between the adrenergic and cholinergic nerves in the rat heart. 2. The negative chronotropic response of the heart rate, evoked by electrical stimulation of the vagus nerve in the pithed rat, was enhanced when the sympathetic cardio-accelerator nerves were stimulated simultaneously. 3. The negative chronotropic response of the heart rate, evoked by electrical stimulation of the vagus nerve in the anaesthetised rat, was inhibited by clonidine and potentiated by a combination of yohimbine and prazosin. A. Field stimulation of rat, isolated, spontaneously beating paired atria resulted in a complex post-stimulus response. The initial negative inotropic component of this response was abolished by atropine. The positive inotropic component of this response was inhibited by propranolol and guanethidine. Atropine and yohimbine both potentiated the positive inotropic component. Clonidine inhibited the positive inotropic component only in the presence of atropine. 5. Clonidine and acetylcholine inhibited the field stimulation- evoked overflow of 3H from atria previously incubated in [3H]-NA. Yohimbine and atropine potentiated the overflow of 3H from such atria. 6. Clonidine and acetylcholine inhibited the field stimulation-evoked overflow of from atria previously incubated in [14C]-choline. Atropine and yohimbine potentiated the overflow of from such atria. The results suggest that field stimulation of atria causes the simultaneous release of NA and ACh and that these transmitters neuromodulate each others release. 7. Part of the study investigated the role of cyclic nucleotides in governing the field stimulation-evoked release of NA and ACh from rat atria. 8. Isobutylmethylxanthine potentiated the field stimulation-evoked overflow of 3H from atria previously incubated in [3H]-NA. 9. In the absence and in the presence of atropine, 8-Bromo-cAMP potentiated the field stimulation-evoked overflow of 3H from atria previously incubated in [3H]-NA. 10. Sodium nitroprusside and 8-Bromo-cGMP both potentiated the field stimulation-evoked overflow of 3H from atria previously incubated in [3H]-NA. In the presence of atropine, sodium nitroprosside was unable to potentiate 3H overflow. 11. Sodium nitroprusside inhibited the field stimulation-evoked overflow of 14C from atria previously incubated in [14 C-choline in the absence and in the presence of prazosin and yohimbine. The results suggest that sodium nitroprusside indirectly potentiated the overflow of 3H by removing the cholinergic-mediated restraint on NA release. 12. In the pithed rat, sodium nitroprusside inhibited the negative chronotropic response of the heart rate evoked by electrical stimulation of the vagus nerve. In the anaesthetised rat, sodium nitroprusside inhibited the same response but this required the presence of prazosin and yohimbine. 13. Part of the study investigated the effects of chronically treating rats with thyroxine (T4). The level of T4 in the serum was increased in rats pretreated with T4, and this was accompanied by changes in pre- and post-synaptic receptor sensitivity. 14. Pretreatment with T4 produced a postsynaptic supersensitivity to isoprenaline amd a postsynaptic subsensitivity to phenylephrine. A presynaptic subsensitivity to clonidine, but not to ACh, was produced by T4 pretreatment. In these pretreated animals the ability of clonidine but not that of ACh to inhibit the field stimulation-evoked overflow of 3H was diminished.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.796056  DOI: Not available
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