Long-term effects of brief antihypertensive treatment on systolic blood pressure and vascular reactivity in young genetically hypertensive rats
dc.contributor.author | Traub, Oren | en_US |
dc.contributor.author | Lloyd, Mary C. | en_US |
dc.contributor.author | Webb, R. Clinton | en_US |
dc.date.accessioned | 2006-09-11T15:05:21Z | |
dc.date.available | 2006-09-11T15:05:21Z | |
dc.date.issued | 1995-06 | en_US |
dc.identifier.citation | Traub, Oren; Lloyd, Mary C.; Webb, R. Clinton; (1995). "Long-term effects of brief antihypertensive treatment on systolic blood pressure and vascular reactivity in young genetically hypertensive rats." Cardiovascular Drugs and Therapy 9(3): 421-429. <http://hdl.handle.net/2027.42/44642> | en_US |
dc.identifier.issn | 0920-3206 | en_US |
dc.identifier.issn | 1573-7241 | en_US |
dc.identifier.uri | https://hdl.handle.net/2027.42/44642 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=8527352&dopt=citation | en_US |
dc.description.abstract | Recent studies have shown that angiotensin converting enzyme (ACE) inhibitor treatment in young spontaneously hypertensive rats (SHR) reduces blood pressure into adulthood. This study explored changes in vascular reactivity in adult normotensive (WKY) rats and stroke-prone SHR (SHRSP) receiving the following treatments at 6–10 weeks of age: (a) ACE inhibitor (ramipril); (b) hydralazine/hydrochlorothiazide (hydral/HCTZ); or (c) no treatment. The hypothesis tested was that vascular changes and blood pressure would be reduced in adult SHRSP treated with ramipril during development. At 17 weeks of age, rats were anesthetized and vascular tissue was excised. Isolated experiments in the aorta included characterization of initial phasic and tonic contractions to 0.1 µM angiotensin II (AII). A phenylephrine (PE) concentration-response curve was performed on carotid arteries, and threshold values were determined. All WKY groups showed lower systolic blood pressure (131±4 mmHg) and reduced phasic AII induced contraction (7.4±4.7%) compared with SHRSP (217±4 mmHg; 37.2±4%). Antihypertensive treatment reduced blood pressure (ramipril: 168±2; hydral/HCTZ: 198±6 mmHg) but not phasic AII responses in adult SHRSP; adult WKY rats were unaffected by treatment. Threshold values for PE in carotid arteries were lower in SHRSP than in WKY, indicating increased sensitivity. However, SHRSP treated with ramipril did not demonstrate increased sensitivity to PE. These data support the hypothesis that blood pressure and sensitivity to PE but not contractile responsiveness to AII in adult SHRSP are determined by an AII-sensitive mechanism during development. | en_US |
dc.format.extent | 1003932 bytes | |
dc.format.extent | 3115 bytes | |
dc.format.mimetype | application/pdf | |
dc.format.mimetype | text/plain | |
dc.language.iso | en_US | |
dc.publisher | Kluwer Academic Publishers; Springer Science+Business Media | en_US |
dc.subject.other | Medicine & Public Health | en_US |
dc.subject.other | Cardiology | en_US |
dc.subject.other | ACE Inhibitors | en_US |
dc.subject.other | Adrenergic | en_US |
dc.subject.other | Angiotensin II | en_US |
dc.subject.other | Antihypertensive | en_US |
dc.subject.other | Genetic Hypertension | en_US |
dc.subject.other | Ramipril | en_US |
dc.subject.other | Spontaneously Hypertensive Rats | en_US |
dc.subject.other | Vascular Smooth Muscle | en_US |
dc.title | Long-term effects of brief antihypertensive treatment on systolic blood pressure and vascular reactivity in young genetically hypertensive rats | en_US |
dc.type | Article | en_US |
dc.subject.hlbsecondlevel | Chemistry | en_US |
dc.subject.hlbsecondlevel | Biological Chemistry | en_US |
dc.subject.hlbtoplevel | Health Sciences | en_US |
dc.subject.hlbtoplevel | Science | en_US |
dc.description.peerreviewed | Peer Reviewed | en_US |
dc.contributor.affiliationum | Department of Physiology, The University of Michigan, 7813 Medical Science Building II, 48109-0622, Ann Arbor, MI | en_US |
dc.contributor.affiliationum | Department of Physiology, The University of Michigan, 7813 Medical Science Building II, 48109-0622, Ann Arbor, MI | en_US |
dc.contributor.affiliationum | Department of Physiology, The University of Michigan, 7813 Medical Science Building II, 48109-0622, Ann Arbor, MI | en_US |
dc.contributor.affiliationumcampus | Ann Arbor | en_US |
dc.identifier.pmid | 8527352 | en_US |
dc.description.bitstreamurl | http://deepblue.lib.umich.edu/bitstream/2027.42/44642/1/10557_2004_Article_BF00879031.pdf | en_US |
dc.identifier.doi | http://dx.doi.org/10.1007/BF00879031 | en_US |
dc.identifier.source | Cardiovascular Drugs and Therapy | en_US |
dc.owningcollname | Interdisciplinary and Peer-Reviewed |
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