Skøtt O, Baumbach L
Pflugers Arch. 1985 Jul;404(3):232-7. doi: 10.1007/BF00581244.
Adenosine produced by the macula densa cells in response to changes in the tubular NaCl-concentration has been suggested to inhibit renin release in vivo. In order to test this suggestion we studied: incubated kidney cortical slices (KS) which contain both the macula densa and the entire afferent arteriole; superfused single microdissected glomeruli (LAG) without macula densa but with the afferent arteriole preserved; and superfused batches of selected glomeruli (SAG) containing only the juxtaglomerular cells closest to the glomerulus. For superfusion and incubation a bicarbonate Ringer solution was used. The specificity of the renin release process was validated by measuring adenylate kinase as a marker for cytoplasmatic leak. Adenosine (10 micrograms/ml) halved basal renin release from incubated KS as compared to controls (P less than 0.001, n = 8, 8). Renin release from LAG stimulated by calcium depletion was also inhibited (P less than 0.05, n = 8, 9) whereas basal release was not affected (n = 6, 12). No effect was detected neither on basal nor on calcium stimulated renin release from SAG. We conclude that adenosine inhibits renin release in vitro by a mechanism independent of a functioning nephron, and which involves only the JG-cells located in the afferent arteriole at some distance from the glomerulus.
致密斑细胞根据肾小管中氯化钠浓度的变化产生的腺苷,被认为在体内可抑制肾素释放。为了验证这一观点,我们进行了以下研究:培养包含致密斑和整个入球小动脉的肾皮质切片(KS);对未含致密斑但保留了入球小动脉的单个显微解剖肾小球(LAG)进行灌流;以及对仅包含最靠近肾小球的球旁细胞的选定肾小球批次(SAG)进行灌流。灌流和培养均使用碳酸氢盐林格溶液。通过测量腺苷酸激酶作为细胞质渗漏的标志物,验证了肾素释放过程的特异性。与对照组相比,腺苷(10微克/毫升)使培养的KS的基础肾素释放减半(P<0.001,n = 8, 8)。钙耗竭刺激的LAG的肾素释放也受到抑制(P<0.05,n = 8, 9),而基础释放不受影响(n = 6, 12)。未检测到腺苷对SAG的基础肾素释放或钙刺激的肾素释放有影响。我们得出结论,腺苷在体外通过一种独立于功能性肾单位的机制抑制肾素释放,该机制仅涉及位于距肾小球一定距离的入球小动脉中的球旁细胞。