Role of calcium ions in the pressure control of renin secretion from the kidneys
Role of calcium ions in the pressure control of renin secretion from the kidneys
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钙离子在肾脏肾素分泌压力控制中的作用
DOI：
10.1007/bf00374855
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
A. Kurtz
中科院分区：
文献类型：
--
作者：
H. Scholz;M. Hamann;K. Götz;A. Kurtz
在这项研究中，我们研究了钙离子的作用，在控制肾素释放的肾动脉压力。为此目的，在压力为140、100、80和40 mmHg [19、13、11、5 kPa]的离体大鼠肾脏中，用含1.5 mmol/l（“正常”）或0钙浓度（含0.5 mmol/l EGTA的无钙灌注液）的培养基灌注，测定肾素分泌率（RSR）。在正常钙的RSR呈负相关的肾动脉压，而钙撤退导致RSR和灌注压之间几乎呈线性和成比例的关系。因此，无钙培养基在140 mmHg（19 kPa）下的RSR与正常钙培养基在40 mmHg（5 kPa）下的肾素释放相似。一氧化氮（NO）供体硝普钠（1 μmol/l）在钙离子浓度为1.5mmol/l时以压力依赖性方式刺激RSR。在无钙灌注液中，硝普钠不能恢复正常钙时RSR的反向压力依赖性，但在整个压力范围内RSR几乎增加了一倍。虽然RSR显着降低血管紧张素II（1 nmol/l）在40毫米汞柱和140毫米汞柱（5-19千帕）与正常钙的范围内，细胞外钙离子的撤出实际上取消了血管紧张素II的抑制作用。由于血管紧张素II衰减RSR，特别是在低肾灌注压，我们的研究结果表明，在这个压力范围内的肾素释放仍然是可接受的钙动员肾肾小球细胞。因此，在较低的压力下，肾素分泌的增强不能用肾素释放对钙离子的敏感性降低来解释。相反，我们的数据支持这样的假设，即“压力感受器”对肾素分泌的控制是通过压力相关的钙内流机制维持的，该机制进入近球细胞，抵消了局部释放的NO的刺激作用。
In this study we examined the role of calcium ions in the control of renin release by the renal artery pressure. For this purpose renin secretion rates (RSR) were measured in isolated rat kidneys perfused at pressures of 140, 100, 80 and 40 mmHg [19, 13, 11, 5 kPa) with media containing either 1.5 mmol/l (“normal”) or zero calcium concentrations (calcium-free perfusate with 0.5 mmol/l EGTA). At normal calcium the RSR was inversely related to the renal artery pressure, whereas calcium withdrawal resulted in an almost linear and proportional relationship between RSR and perfusion pressure. As a consequence, RSR at 140 mmHg (19 kPa) with a calcium-free medium was similar to renin release at 40 mmHg (5 kPa) with normal calcium. The nitric oxide (NO) donor sodium nitroprusside (1 μmol/l) stimulated RSR in a pressure-dependent fashion at a calcium concentration of 1.5 mmol/l. With a calcium-free perfusate, sodium nitroprusside did not restore the inverse pressure dependence of RSR seen with normal calcium but almost doubled the RSR across the whole pressure range. Whilst RSR was significantly reduced by angiotensin II (1 nmol/l) in the range between 40 mmHg and 140 mmHg (5–19 kPa) with normal calcium, withdrawal of extracellular calcium ions practically abolished the inhibitory action of angiotensin II. Since angiotensin II attenuated RSR especially at low renal perfusion pressure, our results indicate that renin release in this pressure range is still inhibitable by calcium mobilization in renal juxtaglomerular cells. Thus, the enhancement of renin secretion at lower pressures cannot be explained by a decreased sensitivity of renin release towards calcium ions. Instead, our data support the hypothesis that the “baroreceptor” control of renin secretion is maintained through a pressure-related calcium influx mechanism into juxtaglomerular cells which counteracts the stimulatory effect of locally released NO.
藤壶肌纤维中细胞内锂激活 Na-H 交换。
DOI：
10.1152/ajpcell.1992.263.1.c246
发表时间：
1992
期刊：
The American journal of physiology
影响因子：
--
作者：
Davis,BA;Hogan,EM;Boron,WF
通讯作者：
Boron,WF
离体微灌注兔传入小动脉中内皮衍生舒张因子对血管紧张素 II 诱导的血管收缩的调节。
DOI：
10.1172/jci115181
发表时间：
1991
期刊：
The Journal of clinical investigation
影响因子：
--
作者：
Ito,S;Johnson,CS;Carretero,OA
通讯作者：
Carretero,OA
影响因子：
4.8
作者：
I. Antonipillai;Richard Horton
通讯作者：
I. Antonipillai;Richard Horton