Yanagisawa H, Morrissey J, Morrison A R, Purkerson M L, Klahr S
Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110.
Am J Physiol. 1990 Jan;258(1 Pt 2):F85-93. doi: 10.1152/ajprenal.1990.258.1.F85.
The production of prostaglandin (PG) E2, 6-keto-PGF1 alpha, and thromboxane B2 (TxB2) under basal conditions and after exposure to angiotensin II (ANG II) or arginine vasopressin (AVP) was examined in vitro in isolated glomeruli. The glomeruli were obtained from control rats and rats with bilateral ureteral obstruction (BUO) of 24-h duration that were pretreated or not with an inhibitor of the angiotensin I converting enzyme (ACE). Basal prostanoid production was greater in isolated glomeruli from BUO rats than in controls. Administration of an ACE inhibitor, enalaprilat, given in vivo returned basal prostanoid production by isolated glomeruli of BUO rats to levels seen in glomeruli of control rats. The prostanoid production in response to addition of ANG II or AVP in vitro was blunted in glomeruli from BUO rats, but the response was restored to "normal" after blockade of ANG II synthesis in vivo in BUO rats. Blockade of ANG II synthesis in vivo did not affect prostanoid synthesis by isolated glomeruli of control rats. The prostanoid generation in response to addition of both ANG II and arachidonic acid in vitro compared with ANG II addition alone was not significantly stimulated in glomeruli from BUO rats. In contrast, it was significantly stimulated in glomeruli of control rats. The results indicate that endogenous ANG II has an important role in the increased synthesis of prostanoids found in isolated glomeruli of rats with BUO and that the in vitro prostanoid production in response to ANG II and AVP can be restored to normal when the synthesis of ANG II is inhibited in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)
在体外对分离的肾小球进行研究，检测基础条件下以及暴露于血管紧张素II（ANG II）或精氨酸加压素（AVP）后前列腺素（PG）E2、6-酮-前列腺素F1α和血栓素B2（TxB2）的生成情况。肾小球取自对照大鼠以及双侧输尿管梗阻（BUO）24小时的大鼠，这些大鼠在预处理或未预处理的情况下使用了血管紧张素I转换酶（ACE）抑制剂。与对照相比，来自BUO大鼠的分离肾小球基础类前列腺素生成更高。给予血管紧张素转换酶抑制剂依那普利拉可使BUO大鼠分离肾小球的基础类前列腺素生成恢复到对照大鼠肾小球的水平。体外添加ANG II或AVP后，BUO大鼠肾小球的类前列腺素生成受到抑制，但在体内阻断BUO大鼠的ANG II合成后，反应恢复到“正常”。体内阻断ANG II合成不影响对照大鼠分离肾小球的类前列腺素合成。与单独添加ANG II相比，体外同时添加ANG II和花生四烯酸后，BUO大鼠肾小球的类前列腺素生成未受到显著刺激。相比之下，对照大鼠肾小球的类前列腺素生成受到显著刺激。结果表明，内源性ANG II在BUO大鼠分离肾小球中类前列腺素合成增加中起重要作用，并且当体内ANG II合成受到抑制时，体外对ANG II和AVP的类前列腺素生成反应可恢复正常。（摘要截短于250字）
