Possible role of adenosine in the macula densa mechanism of renin release in rabbits.
Possible role of adenosine in the macula densa mechanism of renin release in rabbits.
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腺苷在兔肾素释放的致密斑机制中的可能作用。
DOI：
10.1172/jci112118
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Murray,RD
中科院分区：
文献类型：
--
作者：
Itoh,S;Carretero,OA;Murray,RD
本研究的目的是检查：（a）腺苷及其类似物对肾素释放的肾小管，肾小球和致密斑的情况下，和（B）腺苷是否可能参与致密斑介导的肾素释放机制的影响。兔传入小动脉（Af）单独和传入小动脉与致密斑附着（Af + MD）的显微解剖和连续两个30分钟的时间内孵育。计算单个小动脉（或具有致密斑的小动脉）的每小时肾素释放速率，并表示为ng AI × h-1 × Af-1（或Af + MD-1）/h（其中AI为血管紧张素I）。Af的基础肾素释放速率为0.69 +/- 0.09 ng AI × h-1 × Af-1/h Af + MD的基础肾素释放速率为0.20 +/- 0.04 ng AI × h-1 × Af + MD-1/h（n = 6），明显下降（P <0.0025）。当腺苷（0.1 μ M）加入到Af中，肾素释放从0.72 +/- 0.16降至0.24 +/- 0.04 ng AI × h-1 × Af-1/h（P小于0.025; n = 9）。然而，当腺苷加入Af + MD时，未观察到肾素释放的显著变化。N6-环己基腺苷（A1腺苷受体激动剂）在0.1 μ M时使Af的肾素释放从0.69 +/- 0.14降低至0.39 +/- 0.12 ng AI × h-1 × Af-1/h（n = 5，P <0.05）。然而，5 '-N-乙基甲酰胺腺苷（A2腺苷受体激动剂）在0.1 μ M或10 μ M时没有作用。茶碱在不阻断磷酸二酯酶但阻断腺苷受体的浓度（10 μ M）下，使Af + MD的肾素释放从0.21 +/- 0.03增加到0.46 +/- 0.08 ng AI × h-1 × Af + MD-1/h（P <0.05; n = 8）。该结果与腺苷通过激活A1腺苷受体减少肾素释放的假设一致，腺苷可能是从致密斑到肾小球细胞的抑制信号。
This study was designed to examine: (a) the effects of adenosine and its analogues on renin release in the absence of tubules, glomeruli, and macula densa, and (b) whether adenosine may be involved in a macula densa-mediated renin release mechanism. Rabbit afferent arterioles (Af) alone and afferent arterioles with macula densa attached (Af + MD) were microdissected and incubated for two consecutive 30-min periods. Hourly renin release rate from a single arteriole (or an arteriole with macula densa) was calculated and expressed as ng AI X h-1 X Af-1 (or Af + MD-1)/h (where AI is angiotensin I). Basal renin release rate from Af was 0.69 +/- 0.09 ng AI X h-1 X Af-1/h (means +/- SEM, n = 16) and remained stable for 60 min. Basal renin release rate from Af + MD was 0.20 +/- 0.04 ng AI X h-1 X Af + MD-1/h (n = 6), which was significantly lower (P less than 0.0025) than that from Af. When adenosine (0.1 microM) was added to Af, renin release decreased from 0.72 +/- 0.16 to 0.24 +/- 0.04 ng AI X h-1 X Af-1/h (P less than 0.025; n = 9). However, when adenosine was added to Af + MD, no significant change in renin release was observed. N6-cyclohexyl adenosine (an A1 adenosine receptor agonist) at 0.1 microM decreased renin release from Af from 0.69 +/- 0.14 to 0.39 +/- 0.12 ng AI X h-1 X Af-1/h (n = 5, P less than 0.05). However, 5'-N-ethylcarboxamide adenosine (an A2 adenosine receptor agonist) either at 0.1 microM or at 10 microM had no effect. Theophylline, at a concentration (10 microM) that does not block phosphodiesterase but does block adenosine receptors, increased renin release from Af + MD from 0.21 +/- 0.03 to 0.46 +/- 0.08 ng AI X h-1 X Af + MD-1/h (P less than 0.05; n = 8). The results are consistent with the hypotheses that adenosine decreases renin release via the activation of A1 adenosine receptors, and that adenosine may be an inhibitory signal from the macula densa to juxtaglomerular cells.Images