Barrett P Q, Kojima I, Kojima K, Zawalich K, Isales C M, Rasmussen H
Biochem J. 1986 Sep 15;238(3):905-12. doi: 10.1042/bj2380905.
If adrenal glomerulosa cells are treated with angiotensin II for a period of 20-30 min, their subsequent response to either a rechallenge with the same concentration of angiotensin II or treatment with BAY K 8644, a calcium channel agonist, differs from the responses of control cells. Perifusion of control cells with 10 nM-angiotensin II leads to an increase in aldosterone secretory rate from 44 +/- 7 to 166 +/- 9 pg/min per 10(6) cells, but perifusion of cells pretreated for a 20 min period with angiotensin II leads to an increase in secretory rate from 51 +/- 9 to 209 +/- 18 pg/min per 10(6) cells. Likewise, treatment of control cells with 10 nM-BAY K 8644 leads to no significant increase in aldosterone secretory rate, but treatment of previously exposed cells to angiotensin II leads to an increase in rate from 51 +/- 9 to 130 +/- 11 pg/min per 10(6) cells. This memory effect is time-dependent in two ways: cells must be exposed to angiotensin II for 20 min or more before it is apparent; the longer the time between removal of angiotensin II and the rechallenge, the less effect these agents have on aldosterone secretory rate. When cells are exposed to angiotensin II for 20 min and then treated with [Sar1,Ala8]angiotensin II, a competitive antagonist of angiotensin II action, the aldosterone secretory rate falls to basal with a half time of 5-7 min. If BAY K 8644 is added simultaneously with [Sar1,Ala8]angiotensin II, the secretory rate falls with a halftime of 35-60 min. BAY K 8644 increases Ca2+ influx rate to the same extent in the presence or absence of [Sar1,Ala8]angiotensin II, and does not alter the effect of either angiotensin II or [Sar1,Ala8]angiotensin II on the production of inositol tris-, bis-, or mono-phosphate. In cells treated with 10 nM-angiotensin II for either 20, 30 or 45 min, the extent of phosphorylation of four cellular proteins is increased. If cells treated for 20 min with angiotensin II are then treated with [Sar1,Ala8]angiotensin II, and examined 15 min later (35 min), there is no longer an increase in the extent of phosphorylation of any of the four proteins. If such cells are then treated with 10 nM-BAY K 8644 and re-examined 5 min later (40 min), all four patients show an increase in the extent of phosphorylation.(ABSTRACT TRUNCATED AT 400 WORDS)
如果用血管紧张素II处理肾上腺球状带细胞20 - 30分钟，随后它们对相同浓度血管紧张素II的再次刺激或用钙通道激动剂BAY K 8644处理的反应，与对照细胞的反应不同。用10 nM血管紧张素II对对照细胞进行灌流，可使醛固酮分泌率从每10(6)个细胞44±7皮克/分钟增加到166±9皮克/分钟，但用血管紧张素II预处理20分钟的细胞灌流后，分泌率从每10(6)个细胞51±9皮克/分钟增加到209±18皮克/分钟。同样，用10 nM BAY K 8644处理对照细胞不会使醛固酮分泌率显著增加，但将先前暴露于血管紧张素II的细胞进行处理后，分泌率从每10(6)个细胞51±9皮克/分钟增加到130±11皮克/分钟。这种记忆效应在两个方面具有时间依赖性：细胞必须暴露于血管紧张素II 20分钟或更长时间才会显现；血管紧张素II去除与再次刺激之间的时间间隔越长，这些试剂对醛固酮分泌率的影响就越小。当细胞暴露于血管紧张素II 20分钟，然后用血管紧张素II作用的竞争性拮抗剂[Sar1,Ala8]血管紧张素II处理时，醛固酮分泌率在5 - 7分钟的半衰期内降至基础水平。如果在加入[Sar1,Ala8]血管紧张素II的同时加入BAY K 8644，分泌率在35 - 60分钟的半衰期内下降。在有或没有[Sar1,Ala8]血管紧张素II的情况下，BAY K 8644使Ca2+内流速率增加到相同程度，并且不改变血管紧张素II或[Sar1,Ala8]血管紧张素II对肌醇三磷酸、二磷酸或单磷酸产生的影响。用10 nM血管紧张素II处理细胞20、30或45分钟后，四种细胞蛋白的磷酸化程度增加。如果用血管紧张素II处理20分钟的细胞随后用[Sar1,Ala8]血管紧张素II处理，并在15分钟后（35分钟）检查，四种蛋白中任何一种的磷酸化程度都不再增加。如果这些细胞随后用10 nM BAY K 8644处理，并在5分钟后（40分钟）重新检查，所有四个样本的磷酸化程度都增加。（摘要截断于400字）
