Jennifer B. Stott
St George's, University of London
17 Papers
42 Citations
Jennifer B. Stott is an academic researcher from St George's, University of London. The author has contributed to research in topics: Mesenteric arteries & Linopirdine. The author has an hindex of 11, co-authored 15 publications. Previous affiliations of Jennifer B. Stott include St. George's University.
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Papers
KCNQ-Encoded Potassium Channels as Therapeutic Targets.
TL;DR: This review covers the main characteristics of these multifunctional and versatile channels with the aim of providing insight into the therapeutic value of targeting these channels.
119
Contribution of Kv7.4/Kv7.5 Heteromers to Intrinsic and Calcitonin Gene-Related Peptide–Induced Cerebral Reactivity
Preet S. Chadha,Thomas A. Jepps,Georgina Carr,Jennifer B. Stott,Hei-Lei Zhu,William C. Cole,Iain A. Greenwood +6 more
TL;DR: Surprisingly, unlike systemic arteries, Kv7 activity in MCAs is not affected by the development of hypertension, and CGRP-mediated vasodilation is well maintained, which means cerebrovascular KV7 channels could be amenable for therapeutic targeting in conditions such as cerebral vasospasm.
86
Contribution of Kv7 channels to natriuretic peptide mediated vasodilation in normal and hypertensive rats.
TL;DR: This study provides the first evidence that natriuretic peptide responses are impaired in hypertension and that recruitment of Kv7 channels is a key component of natriuric peptide–dependent vasodilations.
61
Kv7 Channel Activation Underpins EPAC-Dependent Relaxations of Rat Arteries
TL;DR: EPAC-dependent vasorelaxations occur in part via activation of Kv7 channels, which contributes to the isoproterenol-mediated relaxation in mesenteric, but not renal, arteries.
53
MicroRNA-153 targeting of KCNQ4 contributes to vascular dysfunction in hypertension.
Georgina Carr,Vincenzo Barrese,Jennifer B. Stott,Oleksandr V. Povstyan,Thomas A. Jepps,Hericka B. Figueiredo,Dongling Zheng,Yalda Jamshidi,Iain A. Greenwood,Iain A. Greenwood +9 more
TL;DR: This study is the first to define a role for aberrant miR 153 contributing to the hypertensive state through targeting of KCNQ4 in an animal model of hypertension, raising the possibility of the use of miR153-related therapies in vascular disease.