Neusser M, Tepel M, Zidek W
Medinische Universitäts Poliklinik, University of Münster, Germany.
J Cardiovasc Pharmacol. 1993 May;21(5):749-53. doi: 10.1097/00005344-199305000-00009.
To examine the interaction of protein kinase C (PKC) with agonist-induced calcium fluxes in hypertension, cytosolic free calcium ([Ca2+]i) was measured in vascular smooth muscle cells (vSMC) of normotensive and spontaneously hypertensive rats (SHR) after incubation with phorbol,-12 myristate,-13 acetate (PMA) and application of angiotensin II (AII). To distinguish between calcium influx through voltage-dependent calcium channels and calcium mobilization from intracellular stores, the calcium agonist BayK 8644 was used. Resting [Ca2+]i was 108.0 +/- 10.6 nM (mean +/- SEM, n = 25) in normotensive and 102.0 +/- 11.4 nM (n = 21) in hypertensive cells. After pretreatment with PMA 10(-7) M for 60 min, resting [Ca2+]i of normotensive vSMC increased to 145.0 +/- 13.8 nM (n = 17) while the resting level of the hypertensive cells decreased to 68.0 +/- 2.4 nM (n = 14, p < 0.05 as compared with normotensive cells) in hypertensive vSMC. Maximum increase in [Ca2+]i induced with 10 M AII for normotensive and hypertensive vSMC was similar: 230.5 +/- 34.4 nM (n = 14) and 212.5 +/- 26.7 nM (n = 17). After pretreatment with PMA 10(-7) M, the maximum increase in [Ca2+]i induced by AII in hypertensive cells was limited to 108.0 +/- 6.2 nM (p < 0.05 as compared with normotensive cells), whereas the increase in [Ca2+]i in normotensive vSMC remained the same as before: 211.5 +/- 23.4 nM. After administration of 10(-5) M BayK 8644, [Ca2+]i increased by 54.3 +/- 12.2 nM (n = 4) and 43.4 +/- 17.4 nM (n = 5) in normotensive and hypertensive vSMC, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
为研究蛋白激酶C（PKC）与高血压中激动剂诱导的钙通量之间的相互作用，在用佛波醇-12-肉豆蔻酸酯-13-乙酸酯（PMA）孵育并应用血管紧张素II（AII）后，测量了正常血压大鼠和自发性高血压大鼠（SHR）血管平滑肌细胞（vSMC）中的胞质游离钙（[Ca2+]i）。为区分通过电压依赖性钙通道的钙内流和细胞内钙库的钙动员，使用了钙激动剂BayK 8644。正常血压细胞的静息[Ca2+]i为108.0±10.6 nM（平均值±标准误，n = 25），高血压细胞为102.0±11.4 nM（n = 21）。用10^(-7)M PMA预处理60分钟后，正常血压vSMC的静息[Ca2+]i增加到145.0±13.8 nM（n = 17），而高血压vSMC中高血压细胞的静息水平降至68.0±2.4 nM（n = 14，与正常血压细胞相比，p < 0.05）。10 μM AII诱导的正常血压和高血压vSMC中[Ca2+]i的最大增加相似：分别为230.5±34.4 nM（n = 14）和212.5±26.7 nM（n = 17）。用10^(-7)M PMA预处理后，AII诱导的高血压细胞中[Ca2+]i的最大增加限制为108.0±6.2 nM（与正常血压细胞相比，p < 0.05），而正常血压vSMC中[Ca2+]i的增加与之前相同：211.5±23.4 nM。给予10^(-5)M BayK 8644后，正常血压和高血压vSMC中[Ca2+]i分别增加了54.3±12.2 nM（n = 4）和43.4±17.4 nM（n = 5）。（摘要截断于250字）
