S
Suzanne Oparil
Researcher at University of Alabama at Birmingham
Publications - 941
Citations - 122414
Suzanne Oparil is an academic researcher from University of Alabama at Birmingham. The author has contributed to research in topics: Blood pressure & Angiotensin II. The author has an hindex of 106, co-authored 885 publications receiving 113983 citations. Previous affiliations of Suzanne Oparil include Michigan State University & Oregon Health & Science University.
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Journal ArticleDOI
Atrial natriuretic peptide dose dependently inhibits cardiac remodeling after exposure to pressure overload
TL;DR: Abstract P-147A Key Words: Atrial Natriuretic Peptide, Card cardiac Remodeling, Cardiac Hypertrophy, and Kidney and Hypertension.
Book ChapterDOI
Effects of Sex Steroids in Vascular Injury
Yiu-Fai Chen,Suzanne Oparil +1 more
TL;DR: Emerging evidence suggests that estrogen may be cardioprotective through a combination of mechanisms in the prevention of cardiovascular morbidity and mortality.
Journal ArticleDOI
Catecholamines, Blood Pressure, Renin and Myocardial Function in the Spontaneously Hypertensive Rat
TL;DR: Neither nerve-growth-factor antiserum (NGFAS) administered subcutaneously nor 6-hydroxydopamine administered intraventricularly to immature spontaneously hypertensive rats (SHR) inhibited the development of the hypertensive syndrome, and NGFSA did not affect blood pressure in normotensive Kyoto/Wistar rats.
Journal ArticleDOI
Les inhibiteurs calciques dans les affections cardiovasculaires : Données cliniques issues des études de morbimortalité
Suzanne Oparil,Stephen Bakir +1 more
TL;DR: L'etude Syst-Eur (Systolic Hypertension in Europe) a ete interrompue prematurement car une reduction significative du nombre d'accidents vasculaires cerebraux and d'evenements cardiaques (fatals et non-fatals) a Ete observee chez les patients traites par the nitrendipine par rapport au placebo.
Book ChapterDOI
Hypertension and Sympathetic Nervous System Activity
David A. Calhoun,Suzanne Oparil +1 more
TL;DR: Results support the concept that chronic sympathetic overactivity induces hypertension, as animal and human studies demonstrate that sustained sympathetic stimulation of the kidney promotes sodium and fluid retention and stimulation ofthe heart increases cardiac output.