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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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Body Mass Index Predicts 24-Hour Urinary Aldosterone Levels in Patients With Resistant Hypertension

TL;DR: In both black andwhite patients, aldosterone levels were positively correlated to increasing BMI, with the correlation being more pronounced in black and white men.
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Fibroblast growth factor mediates hypoxia-induced endothelin-A receptor expression in lung artery smooth muscle cells

TL;DR: The results provide novel finding that ET-AR in PASMCs in vitro is unresponsive to hypoxia per se but is robustly simulated by tyrosine kinase receptor-associated growth factors (FGF-1, FGF-2, PDGF-BB) that themselves are stimulated by Hypoxia in lung.
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Atrial natriuretic peptide in acute hypoxia-induced pulmonary hypertension in rats

TL;DR: The data suggest that 1) exogenous ANP blocks the pulmonary pressor response to acute hypoxia via stimulation of cGMP accumulation in the pulmonary vasculature, and 2) endogenous ANP may modulate the subacute, but not acute, phase of hypoxic pulmonary hypertension.
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Hypothalamic microinjection of alpha2-adrenoceptor agonists causes greater sympathoinhibition in spontaneously hypertensive rats on high NaCl diets

TL;DR: It is shown that in NaCl-sensitive spontaneously hypertensive rats (SHR-S) maintained on high NaCl diets, sympathoinhibitory neurons in the anterior hypothalamic area display increased responsiveness to alpha 2-adrenergic receptor stimulation, giving rise to exaggerated depressor responses.
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Bradykinin in the heart: friend or foe?

TL;DR: It is hypothesized that ACE inhibitors exert beneficial effects by inhibiting both circulating and cardiac tissue ACE, thus attenuating unfavorable remodeling of the left ventricle (LV), reducing afterload, and improving the balance between thrombotic and thrombolytic factors.