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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

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, +1 more
- 01 Jan 2000 - 
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

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.