Brent J.F. Hill
This is a likely match — the affiliation was inferred from OpenAlex, ORCID, and web sources but has not been fully confirmed. Treat with appropriate caution.
Professor and Biology Chair
Also affiliated: Iowa State University (1997); East Carolina University (2000); University of Missouri (1998–2003)
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Brent J.F. Hill's research has primarily investigated cardiovascular function and calcium regulation in smooth muscle cells, particularly within swine models. His work has explored the effects of various factors on intracellular calcium levels and coronary artery constriction. This includes studies on the influence of atorvastatin on calcium uptake in diabetic pigs fed an atherogenic diet and the role of estradiol in non-genomic inhibition of coronary constriction. Hill has also examined the expression of functional nucleotide receptors and sarcoplasmic reticulum morphology in dedifferentiated porcine coronary smooth muscle cells.
In addition to his work on cardiovascular physiology, Hill has contributed to educational methodologies, developing classroom techniques to aid student understanding of biochemical concepts like Michaelis-Menten kinetics. His research also extends to evaluating bone strength in animal models, as demonstrated by his study on tibia bone strength in ovariectomized mice. Hill's scholarship metrics include an h-index of 12, with 34 total publications and 399 total citations.
Metrics
- h-index: 11
- Publications: 32
- Citations: 372
Positions
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University of Central Arkansas publications 2006–2026ORCID
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Professor and Biology Chair publications 2006–2026University of Central Arkansas Institution web page
Selected Publications
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Analysis of leg bones of rats exposed to simulated microgravity and space radiation (2019)
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17β‐estradiol reduces Cav1.2 channel abundance and attenuates Ca2+‐dependent contractions in coronary arteries (2017)
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Using three-point bending to evaluate tibia bone strength in ovariectomized young mice (2017)
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Estrogen Induces Coronary Arterial Dilation via Downregulation of Voltage‐gated, Ca 2+ Channels (2015)
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Oestrogen upregulates the sarcoplasmic reticulum Ca2+ ATP ase pump in coronary arteries (2014)
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The sarcoplasmic reticulum enhances voltage‐gated Ca 2+ influx in resistance arteries from ovariectomized mice (680.19) (2014)
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Short‐term estrogen depletion does not promote hypertension in mice (2013)
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In vivo loss of estrogen increases voltage‐gated calcium channel function in mesenteric arterial smooth muscle cells (2013)
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Activation of the ERα and ERβ pathway downregulates voltage‐gated Ca 2+ channels in coronary arteries (2012)
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The estrogen metabolite, 2‐MeOH, induces arterial dilation by increasing BK channel expression (2011)
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Regulation of voltage‐gated calcium channel expression by estrogen (2010)
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Nongenomic inhibition of coronary constriction by 17β-estradiol, 2-hydroxyestradiol, and 2-methoxyestradiol (2010)
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An estrogen metabolite, 2‐methoxyestradiol, promotes coronary artery dilation and inhibits breast cancer proliferation (2009)
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An estrogen‐induced decrease in voltage‐gated calcium channel expression attenuates coronary artery contractility (2008)
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The estrogen metabolite, 2‐methoxyestradiol, attenuates coronary arterial tone by inhibiting the influx of calcium (2007)
Collaboration Network
Top Collaborators
- 17β‐estradiol reduces Cav1.2 channel abundance and attenuates Ca2+‐dependent contractions in coronary arteries
- Estrogen Induces Coronary Arterial Dilation via Downregulation of Voltage‐gated, Ca 2+ Channels
- An estrogen‐induced decrease in voltage‐gated calcium channel expression attenuates coronary artery contractility
- Regulation of voltage‐gated calcium channel expression by estrogen
- In vivo loss of estrogen increases voltage‐gated calcium channel function in mesenteric arterial smooth muscle cells
- Short‐term estrogen depletion does not promote hypertension in mice
- Activation of the ERα and ERβ pathway downregulates voltage‐gated Ca 2+ channels in coronary arteries
- The sarcoplasmic reticulum enhances voltage‐gated Ca 2+ influx in resistance arteries from ovariectomized mice (680.19)
- In vivo loss of estrogen increases voltage‐gated calcium channel function in mesenteric arterial smooth muscle cells
- Nongenomic inhibition of coronary constriction by 17β-estradiol, 2-hydroxyestradiol, and 2-methoxyestradiol
- An estrogen metabolite, 2‐methoxyestradiol, promotes coronary artery dilation and inhibits breast cancer proliferation
- Nongenomic inhibition of coronary constriction by 17β-estradiol, 2-hydroxyestradiol, and 2-methoxyestradiol
- An estrogen metabolite, 2‐methoxyestradiol, promotes coronary artery dilation and inhibits breast cancer proliferation
- A Simple Classroom Teaching Technique To Help Students Understand Michaelis-Menten Kinetics
- An estrogen metabolite, 2‐methoxyestradiol, promotes coronary artery dilation and inhibits breast cancer proliferation
- 17β‐estradiol reduces Cav1.2 channel abundance and attenuates Ca2+‐dependent contractions in coronary arteries
- Regulation of voltage‐gated calcium channel expression by estrogen
- Using three-point bending to evaluate tibia bone strength in ovariectomized young mice
- In vivo loss of estrogen increases voltage‐gated calcium channel function in mesenteric arterial smooth muscle cells
- 17β‐estradiol reduces Cav1.2 channel abundance and attenuates Ca2+‐dependent contractions in coronary arteries
- Activation of the ERα and ERβ pathway downregulates voltage‐gated Ca 2+ channels in coronary arteries
- Estrogen Induces Coronary Arterial Dilation via Downregulation of Voltage‐gated, Ca 2+ Channels
- Estrogen Induces Coronary Arterial Dilation via Downregulation of Voltage‐gated, Ca 2+ Channels
- The estrogen metabolite, 2‐methoxyestradiol, attenuates coronary arterial tone by inhibiting the influx of calcium
- Oestrogen upregulates the sarcoplasmic reticulum Ca2+ ATP ase pump in coronary arteries
- The enhanced endothelin-1-induced contraction in cultured coronary arteries from mature female pigs is not antagonized by 17β-estradiol
- Nongenomic inhibition of coronary constriction by 17β-estradiol, 2-hydroxyestradiol, and 2-methoxyestradiol
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