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David B. Averill

Researcher at Wake Forest University

Publications -  58
Citations -  5098

David B. Averill is an academic researcher from Wake Forest University. The author has contributed to research in topics: Angiotensin II & Angiotensin II receptor type 1. The author has an hindex of 34, co-authored 58 publications receiving 4755 citations. Previous affiliations of David B. Averill include The Commonwealth Medical College & Ross University.

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Effect of angiotensin-converting enzyme inhibition and angiotensin II receptor blockers on cardiac angiotensin-converting enzyme 2.

TL;DR: Although the predominant effect of ACE inhibition may result from the combined effect of reduced Ang II formation and Ang-(1–7) metabolism, the antihypertensive action of AT1 antagonists may in part be due to increased Ang II metabolism by ACE2.
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Upregulation of Angiotensin-Converting Enzyme 2 After Myocardial Infarction by Blockade of Angiotensin II Receptors

TL;DR: Evidence is provided for an effect of angiotensin II blockade on cardiac ACE 2 mRNA that may be due to direct blockade of AT1a receptors or a modulatory effect of increased angiotENSin-(1–7).
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Effects of renin-angiotensin system blockade on renal angiotensin-(1-7) forming enzymes and receptors

TL;DR: The data revealed a role for ACE2 in Ang-(1-7) formation from Ang II in the kidney of normotensive rats as primarily reflected by the increased ACE2 activity measured in renal membranes from the kidneys of rats given either lisinopril or losartan.
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Vasodepressor Actions of Angiotensin-(1–7) Unmasked During Combined Treatment With Lisinopril and Losartan

TL;DR: Results are the first to indicate an important contribution of Ang-(1-7) in mediating the vasodilator effects caused by combined inhibition of angiotensin-converting enzyme and AT1 receptors.
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Angiotensin peptides and baroreflex control of sympathetic outflow: pathways and mechanisms of the medulla oblongata.

TL;DR: Emphasis is placed on the probable components and neural mechanisms of the medullary baroreflex arc that account for the ability of angiotensin peptides to change the sensitivity of the baroreceptor reflex and to shift the barOREceptor reflex control of sympathetic outflow to higher blood pressures in a pressure-independent manner.