2026-09-18T18:31:19Zhttps://wakespace.lib.wfu.edu/server/oai/request

oai:null:10339/372562026-04-21T20:56:52Zcom_10339_14934col_10339_38132

Carver, Kyle 2012-06-12T08:35:47Z 2013-06-12T08:30:11Z 2012 https://wakespace.lib.wfu.edu/handle/10339/37256 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. en Wake Forest University Angiotensin-(1-7) Angiotensin II Hypertension Restenosis Vascular Remodeling VSMC EFFECT OF ANGIOTENSIN PEPTIDES ON VASCULAR REMODELING Dissertation Tallant, Ann Metheny-Barlow, Linda Callahan, Michael Smith, Thomas Physiology and Pharmacology 2013-06-12 restricted