Suzuki N, Ishii Y, Kitamura S
Department of Pulmonary Medicine, Jichi Medical School, Tochigi, Japan.
Prostaglandins Leukot Essent Fatty Acids. 1994 Apr;50(4):193-7. doi: 10.1016/0952-3278(94)90144-9.
To clarify the relationship between cigarette smoking and regulators of vascular tone derived from endothelium, the authors studied the acute and subacute effects of nicotine on endothelin and eicosanoid production by bovine pulmonary artery endothelial cells (BPAEC). The acute effects of nicotine were assessed by measuring the release of endothelin, prostaglandin I2 (PGI2), and thromboxane A2 (TXA2) from BPAEC after their incubation with a medium containing various concentrations of nicotine (10(-9) M - 10(-3) M) for 24 h. The subacute effects were assessed after 1 week's culture of BPAEC in the presence of nicotine (10(-7) M, 10(-3) M). Acute exposure to a high concentration of nicotine (10(-5) M - 10(-3) M) led to a significant inhibition of endothelin production by BPAEC. Nicotine, 10(-3) M, inhibited PGI2 production, but led to release of lactate dehydrogenase. Subacute exposure to nicotine (10(-3) M) also inhibited the production of endothelin and PGI2 by BPEAC. A high concentration of nicotine reduced the production of endothelin and PGI2 by BPAEC, probably due to the cytotoxicity of nicotine. Concentrations of nicotine comparable to the plasma levels of nicotine found in smokers (10(-9) - 10(-6) M) did not affect the release of endothelin and PGI2 from BPAEC. The mechanism of nicotine-induced vasoconstriction may be independent of the release of endothelin or PG derivatives from endothelial cells.
为阐明吸烟与内皮源性血管张力调节因子之间的关系，作者研究了尼古丁对牛肺动脉内皮细胞（BPAEC）产生内皮素和类花生酸的急性和亚急性影响。通过测量BPAEC在含有不同浓度尼古丁（10⁻⁹M - 10⁻³M）的培养基中孵育24小时后内皮素、前列腺素I2（PGI2）和血栓素A2（TXA2）的释放来评估尼古丁的急性影响。在尼古丁（10⁻⁷M，10⁻³M）存在的情况下对BPAEC进行1周培养后评估亚急性影响。急性暴露于高浓度尼古丁（10⁻⁵M - 10⁻³M）导致BPAEC产生内皮素受到显著抑制。10⁻³M的尼古丁抑制PGI2的产生，但导致乳酸脱氢酶的释放。亚急性暴露于尼古丁（10⁻³M）也抑制了BPEAC产生内皮素和PGI2。高浓度尼古丁降低了BPAEC产生内皮素和PGI2的量，这可能是由于尼古丁的细胞毒性。与吸烟者血浆中发现的尼古丁水平相当的尼古丁浓度（10⁻⁹ - 10⁻⁶M）不影响BPAEC释放内皮素和PGI2。尼古丁诱导血管收缩的机制可能独立于内皮细胞释放内皮素或PG衍生物。
