PROSTAGLANDIN SYNTHESIS IN CULTURED CEREBROMICROVASCULAR AND GLIAL CELLS

细胞内前列腺素与血管紧张素和激肽的相互作用已经被证实， 被认为在调节全身血压方面非常重要 并且可能参与大脑微循环的局部调节。 因此，我们认为， 我们研究了血管紧张素（I或II）或缓激肽对 分离培养脑血管内皮细胞前列腺素合成 和平滑肌，并将它们的反应与神经胶质中的反应进行比较。 在每个细胞的培养基中间接测量PGI 2的合成 用（125 I）6-keto-PGF 1 α放射免疫分析法分型。 前列腺素释放的最大刺激在 暴露于血管紧张素（I或II）的平滑肌细胞培养基 或缓激肽。 (The 6-keto-PGF 1 α浓度高达100 倍于基础水平）。 前列腺素的合成 内皮细胞和神经胶质细胞没有明显的影响， 血管紧张素I 然而，前列腺素释放的轻微增强， 每种细胞系在与血管紧张素II或 缓激肽（高于基础水平20-30%）。 这些结果有力地表明，微血管平滑肌 细胞是对胰高血糖素肽最敏感的部位 这种相互作用可能是调节血管 反应性 前列腺素对血管紧张素的低反应性合成 在内皮和神经胶质中观察到的缓激肽表明这些细胞 可能通过使肽失活或 其他机制。 因此，每个细胞都可能对细胞产生影响。 脑微循环通过其独特的和相互关联的行动。

The cellular prostaglandin interaction with angiotensin and kinins has been considered of great importance in the regulation of systemic blood pressure and possibly in local regulation of the brain microcirculation. Therefore, we investigated the effect of angiotensin (I or II) or bradykinin on prostaglandin synthesis in separately cultured cerebrovascular endothelium and smooth muscle, and compared their responses to that in the glia. The synthesis of PGI2 was measured indirectly in the medium of each cell type using radioimmunoassay with (125I) 6-keto-PGF1Alpha. The greatest stimulation of prostaglandin release was observed in the medium of the smooth muscle cells exposed to either angiotensin (I or II) or to bradykinin. (The concentrations of 6-keto-PGF1Alpha were up to 100 times over the basal levels). The synthesis of prostaglandin in endothelium and glia was not significantly affected by the addition of angiotensin I. However, a slight enhancement of prostaglandin release from each cell line was observed after incubation with either angiotensin II or bradykinin (20-30% over basal level). These results strongly indicate that the cerebromicrovascular smooth muscle cells represent the most sensitive site for prostaglandin-peptide interaction which may be responsible for the modulation of vascular reactivity. The less responsive synthesis of prostaglandin to angiotensin and bradykinin observed in endothelium and glia suggests that these cells might serve as protectors of smooth muscle by inactivating peptides or by other mechanisms. Thus, each of the cells might have an influence on the cerebral microcirculation through its distinct and interrelated actions.