Beierwaltes W H, Schryver S, Olson P S, Romero J C
Hypertension. 1981 Nov-Dec;3(6 Pt 2):II-30-4. doi: 10.1161/01.hyp.3.6_pt_2.ii-30.
Glomeruli were isolated from rat kidneys using a passive sieving technique to study the mechanisms of basal and beta-adrenergic stimulated renin release. Glomeruli were enclosed within glass chambers and continuously superfused with Krebs media, or modified Krebs as described below, at a rate of 0.3 ml/min. The chamber effluent was collected in 10-minute fractions and measured for renin concentration (ng angiotensin I (A-1 generated) by radioimmunoassay. Basal renin was approximately 3 ng AI/ml/hr. Beta-adrenergic stimulation with isoproterenol (ISO), 178 micron M, increased renin concentration threefold (11 +/- 2 ng AI). The beta-blocker propranolol at 12 micron M halved ISO-stimulated renin, and at 120 micron M eliminated it. Doubling Krebs sodium concentration (280 mM) had no effect upon basal or ISO-stimulated renin release. Pretreating rast with DOCA and a high salt diet significantly reduced basal and abolished ISO-stimulated renin release. Increasing Krebs calcium (10 mM) did not affect basal but abolished ISO-stimulated renin release. Calcium-free Krebs had no significant effects. Increasing Krebs potassium (50 mM) increased basal renin fourfold (14 ng AI) while the absolute increase from basal due to ISO remained the same (23 ng AI). These results suggest that basal renin and ISO-stimulated renin are released via different mechanisms.
采用被动筛分技术从大鼠肾脏中分离肾小球，以研究基础状态及β-肾上腺素能刺激下肾素释放的机制。将肾小球置于玻璃小室中，以0.3 ml/分钟的速率持续用 Krebs 培养基或如下所述的改良 Krebs 培养基进行灌流。小室流出液每10分钟收集一次，通过放射免疫测定法测定肾素浓度（ng 血管紧张素 I（生成的 A-1））。基础肾素水平约为3 ng AI/毫升/小时。用178 μM 的异丙肾上腺素（ISO）进行β-肾上腺素能刺激，可使肾素浓度增加三倍（11±2 ng AI）。12 μM 的β受体阻滞剂普萘洛尔可使 ISO 刺激的肾素水平减半，而在120 μM 时则可消除这种刺激。将 Krebs 钠浓度加倍（280 mM）对基础或 ISO 刺激的肾素释放均无影响。用 DOCA 和高盐饮食预处理大鼠可显著降低基础肾素水平，并消除 ISO 刺激的肾素释放。增加 Krebs 钙浓度（10 mM）对基础肾素释放无影响，但可消除 ISO 刺激的肾素释放。无钙的 Krebs 培养基无显著影响。将 Krebs 钾浓度增加至50 mM 可使基础肾素增加四倍（14 ng AI），而 ISO 引起的基础肾素绝对增加量保持不变（23 ng AI）。这些结果表明，基础肾素和 ISO 刺激的肾素通过不同机制释放。
