scispace - formally typeset
A

Adrian D. Bonev

Researcher at University of Vermont

Publications -  81
Citations -  10043

Adrian D. Bonev is an academic researcher from University of Vermont. The author has contributed to research in topics: Vasodilation & Vascular smooth muscle. The author has an hindex of 47, co-authored 80 publications receiving 9383 citations. Previous affiliations of Adrian D. Bonev include Oregon Health & Science University.

Papers
More filters
Journal ArticleDOI

Relaxation of arterial smooth muscle by calcium sparks

TL;DR: KCa channels activated by Ca2+ sparks appeared to hyperpolarize and dilate pressurized myogenic arteries because ryanodine and thapsigargin depolarized and constricted these arteries to an extent similar to that produced by blockers of KCa channels.
Journal ArticleDOI

Vasoregulation by the β1 subunit of the calcium-activated potassium channel

TL;DR: It is shown that targeted deletion of the gene for the β1 subunit leads to a decrease in the calcium sensitivity of BK channels, a reduction in functional coupling of calcium sparks to BK channel activation, and increases in arterial tone and blood pressure.
Journal ArticleDOI

Local potassium signaling couples neuronal activity to vasodilation in the brain.

TL;DR: The results support the concept of intercellular K+ channel–to–K+ channel signaling, through which neuronal activity in the form of an astrocytic Ca2+ signal is decoded by astroCytic BK channels, which locally release K+ into the perivascular space to activate SMC Kir channels and cause vasodilation.
Journal ArticleDOI

Elementary Ca2+ signals through endothelial TRPV4 channels regulate vascular function

TL;DR: Results support the concept that Ca2+ influx through single TRPV4 channels is leveraged by the amplifier effect of cooperative channel gating and the high Ca2- sensitivity of IK and SK channels to cause vasodilation.
Journal ArticleDOI

Ca2+ channels, ryanodine receptors and Ca(2+)-activated K+ channels: a functional unit for regulating arterial tone.

TL;DR: Using functional evidence from cardiac myocytes, and histological evidence from smooth muscle, it is explored whether Ca2+ channels, RyR channels, and KCa channels function as a coupled unit, through Ca2- and voltage, to regulate arterial smooth muscle membrane potential and vascular tone.