{"id":{"repo_id":"wfu","oai_identifier":"oai:wakespace.lib.wfu.edu:10339/37256"},"canonical_url":"https://search.dev.ndltd.org/etd/wfu/oai:wakespace.lib.wfu.edu:10339/37256","repository":{"repo_id":"wfu","name":"Wake Forest University","base_url":"https://wakespace.lib.wfu.edu/oai/request"},"display":{"title":"EFFECT OF ANGIOTENSIN PEPTIDES ON VASCULAR REMODELING","abstract":"Cardiovascular disease, including hypertension and coronary artery disease (CAD), accounts for one in every three deaths in the United States with a direct cost estimated at $286 billion each year. Angiotensin II (Ang II), one of the biologically active peptides of the renin-angiotensin system, elicits many maladaptive effects on the cardiovascular system. Over the past two decades, numerous studies demonstrated that the other biologically active angiotensin peptide, angiotensin-(1-7) [Ang-(1-7)], counter-regulates the actions of Ang II. We demonstrated in Ang II-dependent hypertension that Ang-(1-7) prevents structural remodeling of the microcirculation independent of blood pressure. The heptapeptide hormone decreased the Ang II-induced media to lumen ratio (M/L) by 50%, perivascular fibrosis by 24% and interstitial fibrosis by 46%. These structural reductions were associated with a 32.8% decrease in connective tissue growth factor (CTGF), a 43.1% inhibition in phosphorylated Smad 2 and a 66.2% reduction in phosphorylated ERK1/2 in the arteriole wall of the cremaster muscle. Microvascular remodeling was independent of TGF-beta expression. The dual-specificity phosphatase-1 (DUSP-1) was upregulated in Ang-(1-7) treated animals with or without Ang II, suggesting that the heptapeptide prevents microvascular remodeling by dephosphorylating MAP kinase to inhibit downstream signaling pathways.","abstract_html":"Cardiovascular disease, including hypertension and coronary artery disease (CAD), accounts for one in every three deaths in the United States with a direct cost estimated at $286 billion each year. Angiotensin II (Ang II), one of the biologically active peptides of the renin-angiotensin system, elicits many maladaptive effects on the cardiovascular system. Over the past two decades, numerous studies demonstrated that the other biologically active angiotensin peptide, angiotensin-(1-7) [Ang-(1-7)], counter-regulates the actions of Ang II. We demonstrated in Ang II-dependent hypertension that Ang-(1-7) prevents structural remodeling of the microcirculation independent of blood pressure. The heptapeptide hormone decreased the Ang II-induced media to lumen ratio (M/L) by 50%, perivascular fibrosis by 24% and interstitial fibrosis by 46%. These structural reductions were associated with a 32.8% decrease in connective tissue growth factor (CTGF), a 43.1% inhibition in phosphorylated Smad 2 and a 66.2% reduction in phosphorylated ERK1/2 in the arteriole wall of the cremaster muscle. Microvascular remodeling was independent of TGF-beta expression. The dual-specificity phosphatase-1 (DUSP-1) was upregulated in Ang-(1-7) treated animals with or without Ang II, suggesting that the heptapeptide prevents microvascular remodeling by dephosphorylating MAP kinase to inhibit downstream signaling pathways.","abstract_has_math":false,"creators":["Carver, Kyle"],"institution":"Wake Forest University","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2012,"date_issued":"2012","date_published":"2012","updated_at":"2026-07-27T22:01:27Z","subjects":["Angiotensin-(1-7)"],"languages":["en"],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":"http://hdl.handle.net/10339/37256","outbound_label":"Handle","outbound_source":"dc:identifier.uri"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Carver, Kyle"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.accessioned","label":"Dc Date Accessioned","values":["2012-06-12T08:35:47Z"]},{"key":"dc:date.available","label":"Dc Date Available","values":["2013-06-12T08:30:11Z"]},{"key":"dc:date.issued","label":"Date","values":["2012"]},{"key":"dc:publisher","label":"Institution","values":["Wake Forest University"]},{"key":"dc:type","label":"Dc Type","values":["Dissertation"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Angiotensin-(1-7)"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language.iso","label":"Language (ISO)","values":["en"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://hdl.handle.net/10339/37256"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Cardiovascular disease, including hypertension and coronary artery disease (CAD), accounts for one in every three deaths in the United States with a direct cost estimated at $286 billion each year. Angiotensin II (Ang II), one of the biologically active peptides of the renin-angiotensin system, elicits many maladaptive effects on the cardiovascular system. Over the past two decades, numerous studies demonstrated that the other biologically active angiotensin peptide, angiotensin-(1-7) [Ang-(1-7)], counter-regulates the actions of Ang II. We demonstrated in Ang II-dependent hypertension that Ang-(1-7) prevents structural remodeling of the microcirculation independent of blood pressure. The heptapeptide hormone decreased the Ang II-induced media to lumen ratio (M/L) by 50%, perivascular fibrosis by 24% and interstitial fibrosis by 46%. These structural reductions were associated with a 32.8% decrease in connective tissue growth factor (CTGF), a 43.1% inhibition in phosphorylated Smad 2 and a 66.2% reduction in phosphorylated ERK1/2 in the arteriole wall of the cremaster muscle. Microvascular remodeling was independent of TGF-beta expression. The dual-specificity phosphatase-1 (DUSP-1) was upregulated in Ang-(1-7) treated animals with or without Ang II, suggesting that the heptapeptide prevents microvascular remodeling by dephosphorylating MAP kinase to inhibit downstream signaling pathways."]},{"key":"dc:title","label":"Title","values":["EFFECT OF ANGIOTENSIN PEPTIDES ON VASCULAR REMODELING"]}]}],"canonical_facts":{"dc:creator":["Carver, Kyle"],"dc:date.accessioned":["2012-06-12T08:35:47Z"],"dc:date.available":["2013-06-12T08:30:11Z"],"dc:date.issued":["2012"],"dc:description.abstract":["Cardiovascular disease, including hypertension and coronary artery disease (CAD), accounts for one in every three deaths in the United States with a direct cost estimated at $286 billion each year. Angiotensin II (Ang II), one of the biologically active peptides of the renin-angiotensin system, elicits many maladaptive effects on the cardiovascular system. Over the past two decades, numerous studies demonstrated that the other biologically active angiotensin peptide, angiotensin-(1-7) [Ang-(1-7)], counter-regulates the actions of Ang II. We demonstrated in Ang II-dependent hypertension that Ang-(1-7) prevents structural remodeling of the microcirculation independent of blood pressure. The heptapeptide hormone decreased the Ang II-induced media to lumen ratio (M/L) by 50%, perivascular fibrosis by 24% and interstitial fibrosis by 46%. These structural reductions were associated with a 32.8% decrease in connective tissue growth factor (CTGF), a 43.1% inhibition in phosphorylated Smad 2 and a 66.2% reduction in phosphorylated ERK1/2 in the arteriole wall of the cremaster muscle. Microvascular remodeling was independent of TGF-beta expression. The dual-specificity phosphatase-1 (DUSP-1) was upregulated in Ang-(1-7) treated animals with or without Ang II, suggesting that the heptapeptide prevents microvascular remodeling by dephosphorylating MAP kinase to inhibit downstream signaling pathways."],"dc:identifier.uri":["http://hdl.handle.net/10339/37256"],"dc:language.iso":["en"],"dc:publisher":["Wake Forest University"],"dc:subject":["Angiotensin-(1-7)"],"dc:title":["EFFECT OF ANGIOTENSIN PEPTIDES ON VASCULAR REMODELING"],"dc:type":["Dissertation"]},"updated_at":"2026-07-27T22:01:27Z"}