Toda N, Ayaziki K, Okamura T
Department of Pharmacology, Shiga University of Medical Sciences, Ohtsu, Japan.
J Pharmacol Exp Ther. 1990 Jan;252(1):374-9.
In monkey and dog cerebral artery strips, angiotensin (ANG) II (10(-7) M) produced a transient contraction, which was abolished or suppressed by treatment with indomethacin, aspirin, ONO3708, diphloretin phosphate, antagonists of prostaglandins (PGs) and OKY046, a thromboxane A2 synthesis inhibitor, and by endothelium denudation. On the other hand, PGF2 alpha-induced contractions were not influenced by indomethacin and aspirin, but were suppressed by treatment with ONO3708 and OKY046. Treatment with indomethacin or aspirin potentiated the contractile response of monkey mesenteric arteries, whereas treatment with ONO3708 and removal of endothelium did not alter the response significantly. Saralasin abolished the response to ANG II in these arteries. These findings may indicate that ANG II contracts monkey and dog cerebral arteries by activation of ANG II receptors mainly in endothelium, releasing arachidonic acid and synthesizing vasoconstrictor PGs, such as PGF2 alpha, E2, A2 and D2. Involvement of thromboxane A2 is if any minimal. Vasoconstrictor and dilator PGs released by ANG II appear to modify differently the contraction caused by direct actions of the octapeptide on smooth muscle in monkey cerebral and mesenteric arteries.
在猴和犬的脑动脉条中，血管紧张素（ANG）II（10⁻⁷ M）引起短暂收缩，吲哚美辛、阿司匹林、ONO3708、二氢黄酮磷酸酯、前列腺素（PGs）拮抗剂和血栓素A2合成抑制剂OKY046处理以及内皮剥脱可消除或抑制该收缩。另一方面，PGF2α诱导的收缩不受吲哚美辛和阿司匹林影响，但可被ONO3708和OKY046处理抑制。吲哚美辛或阿司匹林处理增强了猴肠系膜动脉的收缩反应，而ONO3708处理和去除内皮对反应无明显改变。沙拉新消除了这些动脉对ANG II的反应。这些发现可能表明，ANG II通过主要激活内皮中的ANG II受体，释放花生四烯酸并合成血管收缩性PGs，如PGF2α、E2、A2和D2，从而使猴和犬的脑动脉收缩。血栓素A2即便有参与，作用也极小。ANG II释放的血管收缩性和舒张性PGs似乎对八肽直接作用于猴脑动脉和肠系膜动脉平滑肌所引起的收缩有不同的调节作用。
