Studies on dopamine involvement in angiotensin II induced thirst
Studies on dopamine involvement in angiotensin II induced thirst
A study has been made of the thirst response following central administration of dipsogens, with particular reference to the polypeptide angiotensin II. The involvement of the neurotransmitter, dopamine, in thisresponse was investigated. Injections of angiotensin II, neurotensin or carbachol into the lateral cerebroventricles of rats stimulated thirst (potency, angiotensin 11 > carbachol> neurotensin). The angiotensin II stimulated drinking was specifically blocked by a variety of angiotensin II analogues and carbachol drinking was blocked specifically by atropine. Both angiotensin II and neurotensin drinking responses were blocked by dopamine antagonists. These results suggest that all three dipsogens stimulate a different receptor mechanism, and raise the possibility that a dopaminergic mechanism is involved in angiotensin II and neurotensin thirst.This observation was extended to a range of classical and atypical neuroleptics, which, when injected intracerebroventricularly (but not intraperitoneally) inhibited angiotensin II but not carbachol responses with an order of potency resembling that of their clinical effectiveness. Of the dopamine agonists, dopamine itself and 2-(N,N dipropyl) amino 5,6 dihydroxy tetralin were weak dipsogens, whilst surprisingly, the potent dopamine agonist 2-amino-6, 7-dihydroxy-1,2,9,4 tetrahydronapthalene (ADTN) stimulated eating. This latter effect was possibly via the release of noradrenaline. The dopamine agonists and antagonists were also tested on another dopaminergic system, the guinea pig blood pressure hypotensive effect, for comparison with the central studies. Manipulation of dopamine levels in the CNS and subsequent examination of the angiotensin II response added weight to the suggestion that dopamine is involved in the effect. For example, 6-hydroxy dopamine lesions of the nigro-striatal dopamine tract (both unilateral and bilateral) reduced dopamine levels and angiotensin II thirst, whilst chronic haloperidol treatment supersensitised dopamine receptors and increased angiotensin II responses. Carbachol thirst was unaltered in these experiments.In summary, angiotensin II appears to stimulate thirst centrally by interaction with specific receptors, and dopamine has a role in the response.
University of Southampton
1979
Sumners, Colin
(1979)
Studies on dopamine involvement in angiotensin II induced thirst.
University of Southampton, Doctoral Thesis.
Record type:
Thesis
(Doctoral)
Abstract
A study has been made of the thirst response following central administration of dipsogens, with particular reference to the polypeptide angiotensin II. The involvement of the neurotransmitter, dopamine, in thisresponse was investigated. Injections of angiotensin II, neurotensin or carbachol into the lateral cerebroventricles of rats stimulated thirst (potency, angiotensin 11 > carbachol> neurotensin). The angiotensin II stimulated drinking was specifically blocked by a variety of angiotensin II analogues and carbachol drinking was blocked specifically by atropine. Both angiotensin II and neurotensin drinking responses were blocked by dopamine antagonists. These results suggest that all three dipsogens stimulate a different receptor mechanism, and raise the possibility that a dopaminergic mechanism is involved in angiotensin II and neurotensin thirst.This observation was extended to a range of classical and atypical neuroleptics, which, when injected intracerebroventricularly (but not intraperitoneally) inhibited angiotensin II but not carbachol responses with an order of potency resembling that of their clinical effectiveness. Of the dopamine agonists, dopamine itself and 2-(N,N dipropyl) amino 5,6 dihydroxy tetralin were weak dipsogens, whilst surprisingly, the potent dopamine agonist 2-amino-6, 7-dihydroxy-1,2,9,4 tetrahydronapthalene (ADTN) stimulated eating. This latter effect was possibly via the release of noradrenaline. The dopamine agonists and antagonists were also tested on another dopaminergic system, the guinea pig blood pressure hypotensive effect, for comparison with the central studies. Manipulation of dopamine levels in the CNS and subsequent examination of the angiotensin II response added weight to the suggestion that dopamine is involved in the effect. For example, 6-hydroxy dopamine lesions of the nigro-striatal dopamine tract (both unilateral and bilateral) reduced dopamine levels and angiotensin II thirst, whilst chronic haloperidol treatment supersensitised dopamine receptors and increased angiotensin II responses. Carbachol thirst was unaltered in these experiments.In summary, angiotensin II appears to stimulate thirst centrally by interaction with specific receptors, and dopamine has a role in the response.
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Published date: 1979
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Local EPrints ID: 463897
URI: http://eprints.soton.ac.uk/id/eprint/463897
PURE UUID: 528c4508-bf74-4e4a-9c49-746730760c58
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Date deposited: 04 Jul 2022 20:58
Last modified: 04 Jul 2022 20:58
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Author:
Colin Sumners
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