Troponin I phosphorylation in spontaneously hypertensive rat heart: effect of beta-adrenergic stimulation.
Troponin I phosphorylation in spontaneously hypertensive rat heart: effect of beta-adrenergic stimulation.
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自发性高血压大鼠心脏中的肌钙蛋白 I 磷酸化：β-肾上腺素能刺激的作用。
DOI：
10.1152/ajpheart.1997.273.3.h1440
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Bond,M
中科院分区：
文献类型：
--
作者：
McConnell,BK;Moravec,CS;Morano,I;Bond,M
我们比较了26周自发性高血压大鼠（SHR）和Wistar-Kyoto对照组（WKY）心脏32 Pi标记的左心室肌细胞的基线和蛋白激酶A（PKA）依赖性肌钙蛋白I（TnI）磷酸化。将TnI磷酸化归一化为不变的肌球蛋白轻链2磷酸化。在SHR和WKY中，TnI磷酸化的基线没有差异，但是用异丙肾上腺素、去甲肾上腺素加哌唑嗪、毛喉素、氯腺苷3 '，5'-环磷酸或3-异丁基-1-甲基黄嘌呤刺激，SHR中TnI磷酸化的增加比WKY中更大。这在磷酸酶抑制剂calyculin A的存在和不存在下都观察到;因此SHR和WKY之间TnI磷酸化的差异不是由于SHR中磷酸酶活性降低。刺激β-肾上腺素能通路后，受磷蛋白磷酸化在SHR和WKY中没有差异，表明观察到的差异可能是特异性的TnI的PKA磷酸化。与WKY相比，SHR中PKA依赖的TnI磷酸化增加导致肌动球蛋白腺苷三磷酸酶活性的Ca 2+敏感性降低。我们的结论是增加PKA依赖的TnI磷酸化的SHR可能有助于受损的反应交感神经刺激。
We compared baseline and protein kinase A (PKA)-dependent troponin I (TnI) phosphorylation in 32Pi-labeled left ventricular myocytes from hearts of 26-wk spontaneously hypertensive rats (SHR) and Wistar-Kyoto controls (WKY). TnI phosphorylation was normalized to myosin light chain 2 phosphorylation, which was invariant. There was no difference in baseline TnI phosphorylation in SHR and WKY, but stimulation with isoproterenol, norepinephrine plus prazosin, forskolin, chloroadenosine 3',5'-cyclic monophosphate, or 3-isobutyl-1-methylxanthine caused a greater increase in TnI phosphorylation in the SHR than in the WKY. This was observed both in the presence and absence of the phosphatase inhibitor calyculin A; thus the differences in TnI phosphorylation between SHR and WKY are not due to decreased phosphatase activity in the SHR. After stimulation of the beta-adrenergic pathway, phospholamban phosphorylation was not different in SHR and WKY, indicating that the observed differences may be specific for PKA phosphorylation of TnI. The increased PKA-dependent TnI phosphorylation in the SHR resulted in decreased Ca2+ sensitivity of actomyosin adenosinetriphosphatase activity as compared with the WKY. We conclude that increased PKA-dependent TnI phosphorylation in the SHR may contribute to the impaired response to sympathetic stimulation.