Forskolin and calcium: interactions in the control of renin secretion and perfusate flow in the isolated rat kidney.
Forskolin and calcium: interactions in the control of renin secretion and perfusate flow in the isolated rat kidney.
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毛喉素和钙：在离体大鼠肾脏中控制肾素分泌和灌注液流量的相互作用。
DOI：
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
C. Park
中科院分区：
文献类型：
--
作者：
J. Fray;C. Park
使用Forskolin（腺苷酸环化酶激活剂）、高浓度K+和高肾灌注压（已知可增加Ca 2+渗透性的操作）以及calmidazolium（钙调蛋白的特异性阻断剂）来研究腺苷3 '，5'-磷酸（环AMP）和Ca 2+相互作用控制离体灌注大鼠肾脏中的肾素分泌和灌注液流量的机制。在含有5 mM-Ca 2+的培养基中，毛喉素以剂量依赖性方式刺激肾素分泌并引起血管舒张。将Ca 2+浓度降低至1.25 mM并不影响肾素刺激反应，但减弱了血管舒张。高K+浓度逆转了毛喉素诱导的肾素分泌和血管舒张。相反，毛喉素逆转高K+诱导的肾素抑制肾素分泌和血管收缩。这些影响的毛喉素和高K+不存在时，Ca 2+被扣留从灌注介质。高肾灌注压也逆转了毛喉素诱导的肾素分泌。钙咪达唑铵阻止了高K+和高灌注压介导的抑制，从而恢复了毛喉素诱导的刺激。钙咪达唑也引起迅速和明显的血管收缩。钙咪达唑鎓诱导的肾素分泌刺激具有Ca 2+依赖性，因为在无Ca 2+的情况下药物无效。另一方面，即使在无Ca 2+的培养基中，也存在迅速和有效的血管收缩。这些结果支持了这样的假设：环磷酸腺苷通过除了降低细胞质Ca 2+浓度之外还降低膜对Ca 2+的渗透性的机制来刺激血管紧张素分泌。高K+和高肾灌注压通过提高膜对Ca 2+的渗透性来抑制肾素分泌，从而提高细胞内Ca 2+浓度，然后通过钙调蛋白依赖性过程抑制肾素分泌。从这些研究中得出的进一步的一般性结论是，膜对Ca 2+的渗透性和细胞Ca 2+浓度在控制肾素分泌和肾血流中具有中心重要性。
Forskolin (activator of adenyl cyclase), high concentrations of K+ and high renal perfusion pressure (manoeuvres known to increase Ca2+ permeability), and calmidazolium (the specific blocker of calmodulin) were used to investigate the mechanisms whereby adenosine 3',5'‐phosphate (cyclic AMP) and Ca2+ interact to control renin secretion and perfusate flow in the isolated perfused rat kidney. Forskolin stimulated renin secretion and caused vasodilation in a dose‐dependent manner in medium containing 5 mM‐Ca2+. Reducing the Ca2+ concentration to 1.25 mM did not affect the renin stimulatory response but blunted the vasodilation. High K+ concentration reversed the forskolin‐induced renin secretion and vasodilation. Conversely, forskolin reversed the high K+‐induced renin inhibition of renin secretion and vasoconstriction. These effects of forskolin and high K+ were absent when Ca2+ was withheld from the perfusion medium. High renal perfusion pressure also reversed the forskolin‐induced renin secretion. Calmidazolium prevented the inhibition mediated by high K+ and high perfusion pressure and thereby restored the forskolin‐induced stimulation. Calmidazolium also caused a prompt and marked vasoconstriction. The calmidazolium‐induced stimulation of renin secretion was Ca2+‐dependent since the drug was ineffective in the absence of Ca2+. On the other hand, the prompt and potent vasoconstriction was present even in the Ca2+‐free medium. These results support the hypothesis that cyclic AMP stimulates renin secretion by a mechanism which involves a lowering of membrane permeability to Ca2+ in addition to lowering cytosolic Ca2+ concentration. High K+ and high renal perfusion pressure inhibit renin secretion by raising the membrane permeability to Ca2+, thereby raising the intracellular Ca2+ concentration which then inhibits renin secretion by a calmodulin‐dependent process. A further general conclusion from these studies is that membrane permeability to Ca2+ and cellular Ca2+ concentration are of central importance in the control of renin secretion and renal blood flow.
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异丙肾上腺素刺激大鼠肾素分泌：Ca 和环 AMP 的第二信使作用。
影响因子：
6.1
作者：
Churchill,PC;Churchill,MC
通讯作者：
Churchill,MC
三氟拉嗪对大鼠肾切片肾素分泌的影响。
DOI：
--
发表时间：
1983
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
Churchill,PC;Churchill,MC
通讯作者：
Churchill,MC
钙控制肾素分泌：Ca2+流入作为抑制信号。
DOI：
10.1152/ajprenal.1981.240.1.f70
发表时间：
1981
期刊：
The American journal of physiology
影响因子：
--
作者：
Park,CS;Han,DS;Fray,JC
通讯作者：
Fray,JC
有证据表明，β1-肾上腺素受体激活介导大鼠体内异丙肾上腺素刺激的肾素分泌。
影响因子：
4.8
作者：
Churchill,PC;Churchill,MC;McDonald,FD
通讯作者：
McDonald,FD
卡咪唑胺抑制骨骼肌肌浆网 CaATP 酶活性。
DOI：
--
发表时间：
1984
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Anderson,KW;Coll,RJ;Murphy,AJ
通讯作者：
Murphy,AJ