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Haralambos Gavras

Researcher at Boston University

Publications -  244
Citations -  9557

Haralambos Gavras is an academic researcher from Boston University. The author has contributed to research in topics: Blood pressure & Angiotensin-converting enzyme. The author has an hindex of 51, co-authored 244 publications receiving 9368 citations. Previous affiliations of Haralambos Gavras include University of Miami & University of Lausanne.

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Evidence for a Gene Influencing Blood Pressure on Chromosome 17: Genome Scan Linkage Results for Longitudinal Blood Pressure Phenotypes in Subjects From the Framingham Heart Study

TL;DR: Using a genome-wide scan, strong evidence is found for a BP quantitative trait locus on chromosome 17, which could extend the understanding of the genetic basis of essential hypertension and have implications for the evaluation and treatment of patients with high BP.
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Oral Angiotensin-Converting Enzyme Inhibitor in Long-Term Treatment of Hypertensive Patients

TL;DR: The results indicate that chronic inhibition of the angiotensin-converting enzyme with an orally active compound offers a new, efficient, and well-tolerated approach to the treatment of hypertension.
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The A2B adenosine receptor protects against inflammation and excessive vascular adhesion

TL;DR: The A2BAR is identified as a new critical regulator of inflammation and vascular adhesion primarily via signals from hematopoietic cells to the vasculature, focusing attention on the receptor as a therapeutic target.
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An angiotensin converting-enzyme inhibitor to identify and treat vasoconstrictor and volume factors in hypertensive patients.

TL;DR: The antihypertensive action of nonapeptide competitive inhibitor of angiotensin-1-converting enzyme was evaluated in 13 hypertensive patients.
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Insulin Infusion in Conscious Dogs: EFFECTS ON SYSTEMIC AND CORONARY HEMODYNAMICS, REGIONAL BLOOD FLOWS, AND PLASMA CATECHOLAMINES

TL;DR: The results show that the vasomotor effects on regional flows are mediated both via adrenergic mechanisms, and in the case of skeletal muscle and kidney, via mechanisms unrelated to sympathetic stimulation.