Phosphatidic acid increases in response to noradrenaline and endothelin-1 in adult rabbit ventricular myocytes.
Phosphatidic acid increases in response to noradrenaline and endothelin-1 in adult rabbit ventricular myocytes.
复制标题
成年兔心室肌细胞对去甲肾上腺素和内皮素-1 的反应导致磷脂酸增加。
DOI：
10.1093/cvr/28.12.1828
复制
发表时间：
1994
影响因子：
10.8
通讯作者：
Corr,PB
中科院分区：
文献类型：
--
作者：
Ye,H;Wolf,RA;Kurz,T;Corr,PB
目的：探讨去甲肾上腺素（NE）和内皮素-1（ET-1）是否能刺激成年兔心室肌细胞内源性磷脂酸的产生。方法：用NE和ET-1刺激兔心室肌细胞后，用Bligh和Dyer法提取总脂质，用薄层层析法分离，用CuSO 4/H3 PO 4光密度法定量磷脂酸。去甲肾上腺素（10 - 5 M）在2分钟时引起磷脂酸快速增加，磷脂酸在10分钟时出现第二次延迟和持续的增加。对去甲肾上腺素的反应（10− 9至10− 5 M）具有浓度依赖性，半最大响应（EC 50）为3.1 × 10− 8 M，最大效应为10− 6 M。α 1肾上腺素能受体阻断剂2-[β-（4-羟苯基）-乙氨甲基]四氢萘酮可消除去甲肾上腺素引起的磷脂酸生成增加，但β肾上腺素能受体阻断剂L-普萘洛尔不影响。磷脂酸的增加也引起兔心室肌细胞对内皮素-1的反应。该反应具有时间和浓度依赖性，在12 min时最大增加，EC505.3 × 10− 9 M，在10− 6 M时最大效应。去甲肾上腺素和内皮素-1刺激磷脂酰-丁醇生产的存在下，丁醇（100 mM），这表明这两种激动剂激活磷脂酶D.结论：去甲肾上腺素在生理浓度elarms的快速和延迟增加磷脂酸在成年兔心室肌细胞。在生理浓度下，内皮素-1也刺激肌细胞中磷脂酸质量的增加，但内皮素-1诱导的增加是双相的，与去甲肾上腺素刺激期间观察到的双相反应相反。磷脂酶D的激活有助于在用去甲肾上腺素或内皮素-1刺激肌细胞期间观察到的磷脂酸的增加。这是第一个证实离体成人心室肌细胞内源性产生磷脂酸的数据.心血管研究1994;28：1828-1834
Objective:The aim was to assess whether noradrenaline and endothelin-1 can stimulate endogenous production of phosphatidic acid in adult ventricular myocytes.Methods:After stimulation of rabbit ventricular myocytes with noradrenaline and endothelin-1, total lipids were extracted using the Bligh and Dyer procedure and separated by thin layer chromatography, and phosphatidic acid was quantified using photodensitometric analysis of visualised lipids with CuSO4/H3PO4.Results:Noradrenaline (10−5M) elicited a rapid increase in phosphatidic acid at 2 min, followed by a decrease at 5 min. A second delayed and sustained increase in phosphatidic acid occurred at 10 min. The response to noradrenaline (10−9to 10−5M) was concentration dependent with a half maximum response (EC50) of 3.1 × 10−8M and the maximum effect at 10−6M. The increase in phosphatidic acid production in response to noradrenaline was abolished by an α1adrenergic receptor blocking agent (2-[β-(4-hydroxyphenyl)-ethylaminomethyl]tetralone) but unaffected by the β adrenergic blocking agent L-propranolol. An increase in phosphatidic acid was also elicited in rabbit ventricular myocytes in response to endothelin-1. The response was time and concentration dependent with the maximal increase at 12 min, EC505.3 × 10−9M, and maximum effect at 10−6M. Both noradrenaline and endothelin-1 stimulated phosphatidyl- butanol production in the presence of butanol (100 mM), indicating that both agonists activate phospholipase D.Conclusions:Noradrenaline at physiological concentrations elicits both a rapid and a delayed increase in phosphatidic acid in adult rabbit ventricular myocytes. Endothelial-1, at physiological concentrations, also stimulates an increase in the mass of phosphatidic acid in myocytes, but the increase induced by endothelin-1 is monophasic, in contrast to the biphasic response seen during stimulation with noradrenaline. Activation of phospholipase D contributes to the increase in phosphatidic acid seen during stimulation of myocytes with either noradrenaline or endothelin-1. These are the first data to characterise endogenous production of phosphatidic acid in isolated adult ventricular myocytes.Cardiovascular Research1994;28:1828-1834