| Actions of angiotensin and lisinopril on thalamic somatosensory neurons in normotensive, non-transgenic and hypertensive, transgenic rats. | |
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MedLine Citation:
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PMID: 9350589 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVE: To investigate the effects of angiotensin II on discharge rates of somatosensory thalamic neurons and whether these effects are altered in hypertensive transgenic rats [TGR(mREN-2)27] and by long-term treatment with the angiotensin converting enzyme inhibitor lisinopril. DESIGN AND METHODS: Three strains of rats anesthetized with urethane were used (normotensive Wistar and Sprague-Dawley rats (SDR), and [TGR(mREN-2)27]). In addition, the effects of lisinopril treatment on SDR and transgenic animals were tested. The neuronal discharge frequency and the pattern were recorded extracellularly, and their behaviors in response to angiotensin and angiotensin antagonists administered iontophoretically were analyzed. RESULTS: Angiotensin-sensitive neurons located in the ventral posteromedial and ventral posterolateral thalamic nuclei, and in the zona incerta were excited mainly by angiotensin II. The increase in the firing rates induced by administration of angiotensin II often coincided with an increase in the number of bursts of discharges. Effects induced by angiotensin II could be blocked by administration of specific antagonists (losartan, PD 123319). Long-term treatment with lisinopril reduced the neuronal responsiveness to angiotensin II in SDR significantly in comparison with that of untreated SDR controls. Lisinopril-treated SDR had a significantly lower responsiveness to angiotensin II than did hypertensive transgenic rats that had been treated with lisinopril. CONCLUSION: The results show for the first time that administration of angiotensin II induced changes in discharge rates of somatosensory neurons, and that long-term administration of lisinopril caused a significant difference between the neuronal responsiveness to angiotensin of normotensive SDR and that of hypertensive transgenic rats. |
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Authors:
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D Albrecht; P Henklein; D Ganten |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of hypertension Volume: 15 ISSN: 0263-6352 ISO Abbreviation: J. Hypertens. Publication Date: 1997 Oct |
Date Detail:
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Created Date: 1997-12-02 Completed Date: 1997-12-02 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8306882 Medline TA: J Hypertens Country: ENGLAND |
Other Details:
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Languages: eng Pagination: 1151-7 Citation Subset: IM |
Affiliation:
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Institute of Physiology, Faculty of Medicine (Charité), Humboldt University, Berlin, Germany. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Angiotensin II
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pharmacology* Angiotensin-Converting Enzyme Inhibitors / pharmacology* Animals Animals, Genetically Modified Antihypertensive Agents / pharmacology Disease Models, Animal Electroencephalography Hypertension / drug therapy, physiopathology* Imidazoles / pharmacology Lisinopril / pharmacology* Losartan / pharmacology Male Neurons, Afferent / drug effects*, physiology Pyridines / pharmacology Rats Rats, Sprague-Dawley Rats, Wistar Thalamus / drug effects*, physiology Vasoconstrictor Agents / pharmacology* |
| Chemical | |
Reg. No./Substance:
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0/Angiotensin-Converting Enzyme Inhibitors; 0/Antihypertensive Agents; 0/Imidazoles; 0/Pyridines; 0/Vasoconstrictor Agents; 11128-99-7/Angiotensin II; 114798-26-4/Losartan; 130663-39-7/PD 123319; 83915-83-7/Lisinopril |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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