Effect of adenosine analogues on tubuloglomerular feedback responses.
Effect of adenosine analogues on tubuloglomerular feedback responses.
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腺苷类似物对肾小球反馈反应的影响。
DOI：
10.1152/ajprenal.1988.255.1.f33
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Schnermann,J
中科院分区：
文献类型：
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作者：
Schnermann,J
腺苷已被调用作为一个可能的介导的血管收缩反应引起通过管球反馈机制。进行这些实验以研究腺苷类似物对停流压力（SFP）反馈响应的幅度的影响。对于对照溶液，顺行灌注期间SFP的最大变化为6.3 +/- 0.34 mmHg。当腺苷1（A1）受体激动剂CHA、CPA或R-PIA以10（-5）M的浓度存在于灌注液中时，SFP反应显著增强，平均为12.6 ± 1.9（P <0.001）、12.6 ± 0.8（P <0.001）和10.3 ± 1.1 mmHg（P <0.02）。在较高浓度的A1类似物中观察到反应减弱。A2受体激动剂NECA在10（-5）M浓度下未显著改变对照反应，但在较高浓度下降低其幅度。在循环流速逐渐增加的过程中，CPA或R-PIA存在时，基本上所有的反应都发生在0-10 nl/min的流速间隔内，而对照小管中最敏感的流速范围在10 - 20 nl/min之间。在10（-4）M呋塞米存在时，SFP反应在对照和含NECA溶液的灌注过程中消失。相比之下，尽管存在呋塞米，但使用CHA或CPA溶液时SFP下降了11.8 +/- 1.26 mmHg和8.7 +/- 1.25 mmHg。在等渗甘露醇溶液中灌注10（-6）M CPA与SFP降低16.3 +/- 1.42 mmHg相关，而单独甘露醇溶液仅使SFP降低0.6 +/- 0.18 mmHg。我们的研究结果表明，管腔管理A1受体类似物增加SFP反馈响应幅度，效果，不需要存在的管腔NaCl信号。
Adenosine has been invoked as a possible mediator of the vasoconstrictor response elicited through the tubuloglomerular feedback mechanism. These experiments were undertaken to study the effect of adenosine analogues on the magnitude of the stop-flow pressure (SFP) feedback response. With a control solution, maximum change of SFP during orthograde perfusion was 6.3 +/- 0.34 mmHg. When the adenosine1 (A1) receptor agonists CHA, CPA, or R-PIA were present in the perfusate in a concentration of 10(-5) M, SFP responses were significantly augmented and averaged 12.6 +/- 1.9 (P less than 0.001), 12.6 +/- 0.8 (P less than 0.001), and 10.3 +/- 1.1 mmHg (P less than 0.02), respectively. Diminished responses were seen at higher concentrations of A1 analogues. The A2-receptor agonist NECA did not significantly modify the control response at 10(-5) M, but reduced its magnitude at higher concentrations. During graded increases in loop flow rate essentially all of the response in the presence of CPA or R-PIA occurred in the 0-10 nl/min flow interval, whereas the most sensitive flow rate range in the control tubules was between 10 and 20 nl/min. In the presence of 10(-4) M furosemide SFP responses were abolished during perfusion with the control and NECA-containing solutions. In contrast, SFP fell by 11.8 +/- 1.26 mmHg and 8.7 +/- 1.25 mmHg with CHA or CPA solutions despite the presence of furosemide. Perfusion with 10(-6) M CPA in an isotonic mannitol solution was associated with a decrease of SFP by 16.3 +/- 1.42 mmHg, whereas the mannitol solution alone decreased SFP by only 0.6 +/- 0.18 mmHg. Our results show that luminal administration of A1-receptor analogues increases SFP feedback response magnitude, an effect that does not require the presence of a luminal NaCl signal.