Ca2+ influx mediates enhanced alpha2-adrenergic contraction in aortas from rats treated with NOS inhibitor.
Ca2+ influx mediates enhanced alpha2-adrenergic contraction in aortas from rats treated with NOS inhibitor.
复制标题
Ca2 流入介导用 NOS 抑制剂治疗的大鼠主动脉中增强的 α2 肾上腺素能收缩。
DOI：
10.1152/ajpheart.2001.281.5.h2233
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发表时间：
2001
期刊：
影响因子：
--
通讯作者：
Kanagy,NL
中科院分区：
文献类型：
--
作者：
Mukundan,H;Kanagy,NL
Previously, we reported that aortic segments from rats made hypertensive with the nitric oxide synthase inhibitorNω-nitro-l-arginine (l-NNA) exhibit enhanced contractile sensitivity to both α2-adrenergic receptor (α2-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 andl-NNA-treated rats, contraction to the α2-AR agonist UK-14304 stimulated Ca2+influx but released intracellular Ca2+only in control arteries. UK-14304-induced contraction was blocked by the VDCC antagonist nifedipine in both control andl-NNA aortas but contraction of aortas froml-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 Ca2+influx sensitive to nifedipine only in cells froml-NNA-treated rats. We conclude that α2-AR contraction in the rat aorta is mediated primarily by Ca2+influx and thatl-NNA-induced hypertension increases the dependence of this contraction on VDCCs.
