{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/22683"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/22683","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Isolation and purification of a vascular hyperreactivity factor from rabbit kidney cortex","abstract":"Altered vascular response to agonist has been a consistently observed phenomenon in experimental animal and human hypertension. Much evidence suggests that a circulating factor of renal origin is, in part, responsible for this vascular hyperreactivity. The focus of this study was to isolate, purify and identify a vascular hyperreactivity factor (VHRF) from rabbit kidney cortex. Further studies were performed to define the mechanism of action of the VHRF in muscle.","abstract_html":"Altered vascular response to agonist has been a consistently observed phenomenon in experimental animal and human hypertension. Much evidence suggests that a circulating factor of renal origin is, in part, responsible for this vascular hyperreactivity. The focus of this study was to isolate, purify and identify a vascular hyperreactivity factor (VHRF) from rabbit kidney cortex. Further studies were performed to define the mechanism of action of the VHRF in muscle.","abstract_has_math":false,"creators":["Williams, Warren Jon-Allan"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Molecular and Integrative Physiology","degree_department":null,"school":null,"contributors":["Zehr, John E."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2011,"date_issued":"2011-05-07T13:47:57Z","date_published":"2011-05-07T13:47:57Z","updated_at":"2026-07-22T22:25:20Z","subjects":["Biology, Animal Physiology"],"languages":["eng"],"rights":["Copyright 1990 Williams, Warren Jon-Allan"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["AAI9114464","(UMI)AAI9114464"],"render_values":[{"text":"AAI9114464","href":null,"code":true},{"text":"(UMI)AAI9114464","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/22683","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Zehr, John E."]},{"key":"dc:creator","label":"Author","values":["Williams, Warren Jon-Allan"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2011-05-07T13:47:57Z","10000-01-01","1990"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Molecular and Integrative Physiology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Biology, Animal Physiology"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]},{"key":"dc:rights","label":"Dc Rights","values":["Copyright 1990 Williams, Warren Jon-Allan"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["AAI9114464","(UMI)AAI9114464","http://hdl.handle.net/2142/22683"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Altered vascular response to agonist has been a consistently observed phenomenon in experimental animal and human hypertension. Much evidence suggests that a circulating factor of renal origin is, in part, responsible for this vascular hyperreactivity. The focus of this study was to isolate, purify and identify a vascular hyperreactivity factor (VHRF) from rabbit kidney cortex. Further studies were performed to define the mechanism of action of the VHRF in muscle.","Renal cortical tissue was obtained from euthanized New Zealand White rabbits (Oryctolagus cunniculus). By application of a series of techniques (dialysis, gel and ion exchange chromatography, preparative electrofocusing, HPLC, FAB mass spectrometry, FT infrared spectrometry) an acid stable, low molecular weight (147 daltons) compound with a high (+) charge density was obtained. When injected (10 $\\mu$g, i.v.) into assay rats, this compound amplified the pressor response to fixed dosages (5-10 $\\mu$g) of norepinephrine (NE). Taken together, this compound exhibits nearly identical physical characteristics (acid stability, structure, charge and biological activity) to the naturally occurring polyamine spermidine (145.6 daltons). Moreover, in dose-response experiments, $\\mu$g dosages of spermidine amplified the pressor response to a range (5-25 $\\mu$g) of dosages of NE.","The mechanism of action of spermidine was examined in a series of experiments using frog semitendinosus muscle fibers. Single fibers were isolated, mechanically skinned, suspended between a micrometer and a photoelectric force transducer and immersed in a tissue bath. Fiber diameter was recorded at slack length and then a 10% stretch applied. Initially, fiber tension was induced by depolarization with 92 mM chloride. Tension development was found to be inhibited in a dose-dependent manner by $\\mu$M concentrations of spermidine. However, when fiber tension was induced by 2.5 mM caffeine with $\\mu$M concentrations of spermidine, tension development by caffeine was enhanced compared to control values. When fiber tension was induced incrementally by increasing the calcium concentration (pCa tension curve) the presence of spermidine did not displace the pCa tension curve. These experiments suggest that spermidine is acting on the ryanodine receptor to potentiate calcium release from the sarcoplasmic reticulum and does not act either on the dihydropyridine receptor or the contractible elements of the fiber.","Made available in DSpace on 2011-05-07T13:47:57Z (GMT). No. of bitstreams: 2 license.txt: 4922 bytes, checksum: 910b249b4beec47e7ab768910c8f966f (MD5) 9114464.pdf: 5115848 bytes, checksum: e9e0c4af7ebbfc3589fbb5efec1369cc (MD5) Previous issue date: 1990","Item marked as restricted to the 'UIUC Users [automated]' Group (id=2) by Howard Ding (hding2@illinois.edu) on 2011-05-07T14:59:17Z Item is restricted indefinitely.","Restriction data tranferred 2014-07-01T11:27:57-05:00 Original Data Group with Access UIUC Users [automated] Release Date: none Reason: ETDs are only available to UIUC Users without author permission","ETDs are only available to UIUC Users without author permission","U of I Only"]},{"key":"dc:title","label":"Title","values":["Isolation and purification of a vascular hyperreactivity factor from rabbit kidney cortex"]}]}],"canonical_facts":{"dc:contributor":["Zehr, John E."],"dc:creator":["Williams, Warren Jon-Allan"],"dc:date":["2011-05-07T13:47:57Z","10000-01-01","1990"],"dc:description":["Altered vascular response to agonist has been a consistently observed phenomenon in experimental animal and human hypertension. Much evidence suggests that a circulating factor of renal origin is, in part, responsible for this vascular hyperreactivity. The focus of this study was to isolate, purify and identify a vascular hyperreactivity factor (VHRF) from rabbit kidney cortex. Further studies were performed to define the mechanism of action of the VHRF in muscle.","Renal cortical tissue was obtained from euthanized New Zealand White rabbits (Oryctolagus cunniculus). By application of a series of techniques (dialysis, gel and ion exchange chromatography, preparative electrofocusing, HPLC, FAB mass spectrometry, FT infrared spectrometry) an acid stable, low molecular weight (147 daltons) compound with a high (+) charge density was obtained. When injected (10 $\\mu$g, i.v.) into assay rats, this compound amplified the pressor response to fixed dosages (5-10 $\\mu$g) of norepinephrine (NE). Taken together, this compound exhibits nearly identical physical characteristics (acid stability, structure, charge and biological activity) to the naturally occurring polyamine spermidine (145.6 daltons). Moreover, in dose-response experiments, $\\mu$g dosages of spermidine amplified the pressor response to a range (5-25 $\\mu$g) of dosages of NE.","The mechanism of action of spermidine was examined in a series of experiments using frog semitendinosus muscle fibers. Single fibers were isolated, mechanically skinned, suspended between a micrometer and a photoelectric force transducer and immersed in a tissue bath. Fiber diameter was recorded at slack length and then a 10% stretch applied. Initially, fiber tension was induced by depolarization with 92 mM chloride. Tension development was found to be inhibited in a dose-dependent manner by $\\mu$M concentrations of spermidine. However, when fiber tension was induced by 2.5 mM caffeine with $\\mu$M concentrations of spermidine, tension development by caffeine was enhanced compared to control values. When fiber tension was induced incrementally by increasing the calcium concentration (pCa tension curve) the presence of spermidine did not displace the pCa tension curve. These experiments suggest that spermidine is acting on the ryanodine receptor to potentiate calcium release from the sarcoplasmic reticulum and does not act either on the dihydropyridine receptor or the contractible elements of the fiber.","Made available in DSpace on 2011-05-07T13:47:57Z (GMT). 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