Role of calcium and calmodulin in release of kallikrein and tonin from rat submandibular gland.

Role of calcium and calmodulin in release of kallikrein and tonin from rat submandibular gland.
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钙和钙调蛋白在大鼠颌下腺释放激肽释放酶和色调剂中的作用。

DOI:
10.1152/ajpcell.1986.250.3.c480
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发表时间:
1986
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Rabito,SF
Rabito,SF
中科院分区:
--
文献类型:
--
作者:
Maitra,SR;Carretero,OA;Smith,SW;Rabito,SF

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我们研究了去甲肾上腺素(NE)诱导的激肽释放酶和张力素释放中钙和钙调素作为细胞内介质的作用。我们研究了在有或无钙,两种钙阻滞剂,和四种不同的钙调素拮抗剂的NE反应的大鼠下颌下腺的激肽释放酶和张力素的分泌速率。在体外孵育下颌下腺切片,并通过直接放射免疫测定法测定分泌到孵育培养基中的腺激肽释放酶和紧张素,并表示为纳克/分钟/毫克组织。NE(10(-5)和10(-4)M)使激肽释放酶分泌从对照值8.2 +/- 2.6增加到134.9 +/- 41.4(P <0.05)和191.2 +/- 62.7(P小于0.05),并且张力素的释放从3.5 +/- 0.6的基础速率到51.5 +/- 9.1(P小于0.05)和64.4 +/- 13.7(P小于0.05)。去钙和加入EGTA的孵育液显着减弱了NE诱导的激肽释放酶和张力素的分泌。硝苯地平在抑制电压依赖性钙通道的浓度下,不影响激肽释放酶和张力素的释放,只有高浓度(10(-4)M)才能减少释放。TMB-8,一种细胞内钙离子的阻滞剂,也没有影响。吩噻嗪类药物三氟丙嗪(10(-6)M)和三氟拉嗪(10(-4)M)显著降低10(-5)M NE引起的激肽释放酶释放。(250字处删节)
We investigated the role of calcium and calmodulin as intracellular mediators of kallikrein and tonin release induced by norepinephrine (NE). We studied the secretion rate of kallikrein and tonin from submandibular gland of rat in response to NE in the presence or absence of calcium, two calcium blockers, and four different calmodulin antagonists. Submandibular gland slices were incubated in vitro, and glandular kallikrein and tonin secreted into the incubation medium were determined by direct radioimmunoassays and expressed as nanograms per minute per milligram tissue. NE (10(-5) and 10(-4) M) increased the kallikrein secretion from the control value of 8.2 +/- 2.6 to 134.9 +/- 41.4 (P less than 0.05) and to 191.2 +/- 62.7 (P less than 0.05), and the release of tonin from a basal rate of 3.5 +/- 0.6 to 51.5 +/- 9.1 (P less than 0.05) and to 64.4 +/- 13.7 (P less than 0.05). The deletion of calcium and addition of EGTA into the incubation medium significantly attenuated the secretion of kallikrein and tonin induced by NE. Nifedipine, at concentrations which inhibit voltage-dependent calcium channels, did not affect the release of kallikrein and tonin, and only a high concentration (10(-4) M) reduced the release. TMB-8, a blocker of intracellular calcium, had no effect either. Phenothiazines, triflupromazine (10(-6) M) and trifluoperazine (10(-4) M), decreased significantly the kallikrein release elicited by 10(-5) M NE.(ABSTRACT TRUNCATED AT 250 WORDS)