| Nerve growth factor enhances calcitonin gene-related peptide expression in the spontaneously hypertensive rat. | |
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MedLine Citation:
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PMID: 11230364 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Calcitonin gene-related peptide (CGRP) expression is markedly reduced in dorsal root ganglia neurons in the spontaneously hypertensive rat (SHR). This decrease in such a potent vasodilator may contribute to the elevated blood pressure. Therefore, the purpose of this study was to determine whether stimulation of neuronal CGRP expression in SHR, by means of the administration of nerve growth factor, would lower the blood pressure. Nerve growth factor (10 nmol/L per kg/d, IP) was given to 12-week SHR (n=8 to 11/group) once a day for 1, 3, and 7 days. Control SHR received vehicle only. All rats were instrumented for CGRP receptor antagonist (CGRP(8-37)) administration (intravenous) and mean arterial pressure recording. Both the 1- and 3-day NGF treatments lowered the mean arterial pressure to 147+/-5 and 147+/-3 mm Hg, respectively, compared with controls (166+/-3 mm Hg). However, by day 7, the mean arterial pressure had returned to control levels (169+/-5 mm Hg). CGRP(8-37) administration produced a significant mean arterial pressure increase in all 3 nerve growth factor-treated groups (14+/-2, 10+/-2, and 13+/-2 mm Hg). CGRP mRNA levels in dorsal root ganglia were increased in the 3 neurotrophin-treated groups, whereas CGRP peptide content was higher at days 3 and 7. Therefore, nerve growth factor treatment of SHR can enhance neuronal CGRP expression. At days 1 and 3, nerve growth factor produces a depressor response that is primarily mediated by CGRP as evidenced by the pressor effect of CGRP(8-37.) At day 7, CGRP also plays a counterregulatory role, even though the mean arterial pressure has returned to control levels. This finding may result from a nerve growth factor-mediated upregulation of a pressor system that counteracts the hypotensive actions of CGRP. Thus, these data suggest that the decreased production of CGRP in SHR could contribute to the hypertension. |
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Authors:
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S C Supowit; H Zhao; D J DiPette |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Hypertension Volume: 37 ISSN: 1524-4563 ISO Abbreviation: Hypertension Publication Date: 2001 Feb |
Date Detail:
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Created Date: 2001-03-20 Completed Date: 2001-04-26 Revised Date: 2013-03-18 |
Medline Journal Info:
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Nlm Unique ID: 7906255 Medline TA: Hypertension Country: United States |
Other Details:
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Languages: eng Pagination: 728-32 Citation Subset: IM |
Affiliation:
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Michigan State University, College of Human Medicine, Department of Medicine, East Lansing, Michigan, USA. scott.supowit@ht.msu.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Blood Pressure / drug effects Blotting, Northern Calcitonin Gene-Related Peptide / biosynthesis*, genetics, pharmacology Ganglia, Spinal / metabolism* Hypertension / etiology Male Nerve Growth Factor / pharmacology* Neurons / metabolism Peptide Fragments / pharmacology RNA, Messenger / biosynthesis Radioimmunoassay Rats Rats, Inbred SHR Receptors, Calcitonin Gene-Related Peptide / antagonists & inhibitors Time Factors Up-Regulation |
| Grant Support | |
ID/Acronym/Agency:
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HL-44277/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Peptide Fragments; 0/RNA, Messenger; 0/Receptors, Calcitonin Gene-Related Peptide; 119911-68-1/calcitonin gene-related peptide (8-37); 83652-28-2/Calcitonin Gene-Related Peptide; 9061-61-4/Nerve Growth Factor |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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