English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Previously, we reported that aortic segments from rats made hypertensive with the nitric oxide synthase inhibitor N  ω -nitro-l-arginine (l-NNA) exhibit enhanced contractile sensitivity to both α 2 -adrenergic receptor (α 2 -AR) stimulation and to KCl-induced depolarization. We hypothesized that increased contractile responses to these agents was due to a change in the common effector L-type voltage-dependent calcium channel (VDCC). In aortic segments from control and l-NNA-treated rats, contraction to the α 2 -AR agonist UK-14304 stimulated Ca 2+ influx but released intracellular Ca 2+  only in control arteries. UK-14304-induced contraction was blocked by the VDCC antagonist nifedipine in both control and l-NNA aortas but contraction of aortas from l-NNA-treated rats was blocked by lower concentrations. Calcium imaging studies in fura 2-loaded freshly isolated aortic vascular smooth muscle cells also demonstrated UK-14304-stimulated Ca 2+  influx sensitive to nifedipine only in cells from l-NNA-treated rats. We conclude that α 2 -AR contraction in the rat aorta is mediated primarily by Ca 2+  influx and that l-NNA-induced hypertension increases the dependence of this contraction on VDCCs.

Ca2+influx mediates enhanced α2-adrenergic contraction in aortas from rats treated with NOS inhibitor

Ca²⁺influx mediates enhanced α₂-adrenergic contraction in aortas from rats treated with NOS inhibitor