M
Marie L. Steenberg
Researcher at University of Houston
Publications - 17
Citations - 330
Marie L. Steenberg is an academic researcher from University of Houston. The author has contributed to research in topics: Cardiac output & Stimulation. The author has an hindex of 9, co-authored 17 publications receiving 330 citations. Previous affiliations of Marie L. Steenberg include National Institutes of Health & University of Nigeria, Nsukka.
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Journal ArticleDOI
Effects of several tricyclic antidepressants on the hemodynamics and myocardial contractility of the anesthetized dogs.
Bhagavan S. Jandhyala,Bhagavan S. Jandhyala,Marie L. Steenberg,Marie L. Steenberg,James M. Perel,James M. Perel,Albert A. Manian,Albert A. Manian,Joseph P. Buckley,Joseph P. Buckley +9 more
TL;DR: The results of this investigation demonstrated that the complex cardiovascular effects of tricyclic antidepressants observed in these studies were perhaps due to a direct and/or autonomically mediated effects on the heart and vasculature.
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Presynaptic alpha- and beta-adrenoceptor stimulation and norepinephrine release in the spontaneously hypertensive rat.
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Chemistry of the phenoxathiins i. Synthesis of 1-azaphenoxathiin analogs as potential new CNS depressant agents
TL;DR: In this article, the disodium salt of 2-mercapto-3-pyridinol with various ortho-nitrohalo-benzenes to yield a group of previously unreported 1-azaphenoxathiins is described.
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Effect of epinephrine on norepinephrine release from rat kidney during sympathetic nerve stimulation
TL;DR: Results, while providing evidence for the existence of presynaptic facilitatory beta-adrenoceptors on renal sympathetic nerves, fail to support the hypothesis that these receptors have a physiological role in the regulation of sympathetic neurotransmitter release.
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Presynaptic inhibition of sympathetic neurotransmision by adenosine in the rat kidney
TL;DR: The results indicate that adenosine can inhibit sympathetic neurotransmission in the rat kidney through a presynaptic purinergic mechanism as evidenced in a dose-dependent reduction in the vasoconstrictor responses elicit by periarterial nerve stimulation.