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• W2185099184 abstract "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." @default.
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• W2185099184 date "2001-11-01" @default.
• W2185099184 modified "2023-09-25" @default.
• W2185099184 title "Ca²⁺influx mediates enhanced α₂-adrenergic contraction in aortas from rats treated with NOS inhibitor" @default.
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• W2185099184 doi "https://doi.org/10.1152/ajpheart.2001.281.5.h2233" @default.
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