Impact of cyclo-oxygenase blockade on juxtamedullary microvascular responses to angiotensin II in rat kidney.
Impact of cyclo-oxygenase blockade on juxtamedullary microvascular responses to angiotensin II in rat kidney.
复制标题
环加氧酶阻断对大鼠肾脏近髓微血管对血管紧张素 II 反应的影响。
DOI：
10.1111/j.1440-1681.1995.tb01927.x
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发表时间：
1995
影响因子：
2.9
通讯作者：
Carmines,PK
中科院分区：
文献类型：
--
作者：
Harrison-Bernard,LM;Carmines,PK
1. 实验旨在评估环加氧酶产物调节血管紧张素II （AII）对依那普利治疗大鼠肾髓旁微血管的影响。2. 利用体外血灌注髓旁肾元技术，提供位于外髓外条纹的传入小动脉、传出小动脉和降直血管的通路。3. 在环加氧酶阻断（1 μ mol/L吡罗昔康）的肾脏中，基线传入小动脉直径为20.8+/-1.9微米，显著低于未治疗肾脏（26.1+/-1.0微米）。输出小动脉和外髓降血管的基线直径在未治疗组和吡罗昔康治疗组之间没有差异。4. 局部应用1 nmol/L AII可使未治疗肾脏的外髓降血管直肠血流减少22+/-6%，吡罗昔康治疗肾脏的血流减少24+/-7%。5. 在未处理的肾脏中，AII （0.01-100 nmol/L）产生浓度依赖性的传入和输出小动脉收缩反应，其强度相似。在吡罗昔康治疗的肾脏中，传入和传出小动脉AII反应均未发生显著改变，尽管在AII浓度为>或= 10 nmol/L时，传入反应超过传出反应。6. 我们得出结论，内源性环加氧酶产物在基线条件下对髓旁传入小动脉发挥血管扩张作用。虽然环加氧酶抑制对肾小球旁微血管对AII的反应影响不大，但对高浓度AII的反应可能由环加氧酶产物调节，从而微妙地改变肽对肾小球前和肾小球后抵抗的相对影响。
1. Experiments were designed to evaluate the hypothesis that cyclo-oxygenase products modulate the influence of angiotensin II (AII) on the renal juxtamedullary microvasculature of enalaprilat-treated rats. 2. The in vitro blood-perfused juxtamedullary nephron technique was utilized to provide access to afferent arterioles, efferent arterioles and descending vasa recta located in the outer stripe of the outer medulla. 3. Baseline afferent arteriolar diameter was 20.8+/-1.9 microns in kidneys subjected to cyclo-oxygenase blockade (1 mumol/L piroxicam), a value significantly lower than that observed in untreated kidneys (26.1+/-1.0 microns). Baseline diameters of efferent arterioles and outer medullary descending vasa recta did not differ between untreated and piroxicam-treated groups. 4. Topical application of 1 nmol/L AII reduced blood flow through outer medullary descending vasa recta by 22+/-6% in untreated kidneys and by 24+/-7% in piroxicam-treated kidneys. 5. In untreated kidneys, AII (0.01-100 nmol/L) produced concentration-dependent afferent and efferent arteriolar constrictor responses of similar magnitudes. Neither afferent nor efferent arteriolar AII responsiveness was significantly altered in piroxicam-treated kidneys, although afferent responses exceeded efferent responses at AII concentrations> or= 10 nmol/L. 6. We conclude that endogenous cyclo-oxygenase products exert a vasodilator influence on juxtamedullary afferent arterioles under baseline conditions. Although cyclo-oxygenase inhibition had little effect on juxtamedullary microvascular responses to AII, the response to high AII concentrations may be modulated by cyclo-oxygenase products in a manner which delicately alters the relative influence of the peptide on pre-vs postglomerular resistances.