Effect of parathyroid hormone on rat renal calcium/calmodulin-dependent protein kinase II.

R Nemani, N Wongsurawat, H J Armbrecht
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Abstract

Rat parathyroid hormone (PTH) stimulates cAMP-dependent protein kinase and protein kinase C activity in the kidney. However, PTH increases intracellular Calcium in primary cultures of proximal tubular cells. We have investigated the possibility that PTH also stimulates Calcium/calmodulin-dependent protein kinase II (CaM kinase II). We have employed the tandem chromatographic column method, using synthetic peptide as a substrate, to measure the renal CaM kinase II activity. PTH (250 nM) stimulated CaM kinase II activity by about 50% after 15 sec., and activity returned to baseline by 2 min. Calmodulin antagonists significantly impaired the stimulatory action of PTH whereas basal levels of CaM kinase II activity were relatively unaffected. This study demonstrates that PTH does activate CaM kinase II in renal tissue, and suggests another pathway for the actions of PTH in the kidney.

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甲状旁腺激素对大鼠肾钙/钙调素依赖性蛋白激酶II的影响。
大鼠甲状旁腺激素(PTH)刺激肾camp依赖性蛋白激酶和蛋白激酶C活性。然而,甲状旁腺激素在近端小管细胞的原代培养中增加细胞内钙。我们研究了甲状旁腺素也刺激钙/钙调素依赖性蛋白激酶II (CaM kinase II)的可能性。我们采用串联色谱柱法,使用合成肽作为底物,测量肾脏CaM激酶II的活性。PTH (250 nM)在15秒后刺激了约50%的CaM kinase II活性,并在2分钟后恢复到基线水平。钙调素拮抗剂显著削弱了PTH的刺激作用,而CaM kinase II活性的基础水平相对不受影响。本研究表明PTH确实激活肾组织中的CaM激酶II,并提示PTH在肾脏中的作用的另一途径。
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