Ankorina-Stark I, Haxelmans S, Schlatter E
Medizinische Poliklinik, Westfälische Wilhelms-Universität, Münster, Germany.
Cell Calcium. 1997 Feb;21(2):163-71. doi: 10.1016/s0143-4160(97)90040-3.
In freshly isolated rat CCD segments, the effects of arginine vasopressin (AVP), oxytocin (OT), adrenaline (Ad), and their specific receptor agonists and antagonists on the intracellular Ca2+ activity ([Ca2+]i) were measured using the Ca2+ sensitive dye Fura-2 as fluorescence indicator. We observed that AVP, the V1-receptor agonist [Phe2Orn8] vasotocin ([Phe2]OVT), and OT increased [Ca2+]i biphasically. AVP (n = 9) and OT (n = 8) induced increases in [Ca2+]i were completely blocked by the V1A-receptor antagonist d(CH2)5Tyr(Me)2AVP. However, neither the V2-receptor agonist [Val4-D-Arg8]AVP (100 nM, n = 5), nor the OT-receptor agonist [Thr4,Gly7]OT (100 nM, n = 5) nor forskolin (1 microM, n = 4 and 10 microM, n = 5) did significantly change [Ca2+]i. Ad and the beta-adrenoceptor agonist isoproterenol (ISO) increased [Ca2+]i, which was not mimicked by the alpha 2-adrenoceptor agonist clonidine (1 microM, n = 10) or the alpha 1-adrenoceptor agonist phenylephrine (1 microM, n = 5). The beta-adrenoceptor antagonist propranolol (1 microM) completely blocked this Ad (1 microM, n = 4) induced [Ca2+]i increase. Insulin (INS 10 nM, n = 8), endothelin (ET 1 microM, n = 6), and angiotensin II (Ang II 1 pM to 10 nM; each n = 4) had no significant effect on [Ca2+]i. Considering the present results we propose a V1A-receptor and beta-adrenoceptor dependent modulation of [Ca2+]i in rat CCD.
在新鲜分离的大鼠皮质集合管（CCD）节段中，使用钙敏感染料Fura - 2作为荧光指示剂，测量了精氨酸加压素（AVP）、催产素（OT）、肾上腺素（Ad）及其特异性受体激动剂和拮抗剂对细胞内钙活性（[Ca2 + ]i）的影响。我们观察到，AVP、V1受体激动剂[苯丙氨酸2 - 鸟氨酸8]血管紧张素（[苯丙氨酸2]OVT）和OT使[Ca2 + ]i呈双相增加。AVP（n = 9）和OT（n = 8）诱导的[Ca2 + ]i增加被V1A受体拮抗剂d(CH2)5Tyr(Me)2AVP完全阻断。然而，V2受体激动剂[缬氨酸4 - D - 精氨酸8]AVP（100 nM，n = 5）、OT受体激动剂[苏氨酸4，甘氨酸7]OT（100 nM，n = 5）以及福斯可林（1 μM，n = 4和10 μM，n = 5）均未显著改变[Ca2 + ]i。Ad和β - 肾上腺素能受体激动剂异丙肾上腺素（ISO）使[Ca2 + ]i增加，α2 - 肾上腺素能受体激动剂可乐定（1 μM，n = 10）或α1 - 肾上腺素能受体激动剂去氧肾上腺素（1 μM，n = 5）未模拟此作用。β - 肾上腺素能受体拮抗剂普萘洛尔（1 μM）完全阻断了Ad（1 μM，n = 4）诱导的[Ca2 + ]i增加。胰岛素（INS 10 nM，n = 8）、内皮素（ET 1 μM，n = 6）和血管紧张素II（Ang II 1 pM至10 nM；每组n = 4）对[Ca2 + ]i无显著影响。考虑到目前的结果，我们提出大鼠CCD中[Ca2 + ]i存在V1A受体和β - 肾上腺素能受体依赖性调节。
