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首页> 外文期刊>American Journal of Physiology >Reduction in interaction between cGMP and cAMP in dog ventricular myocytes with hypertrophic failure.
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Reduction in interaction between cGMP and cAMP in dog ventricular myocytes with hypertrophic failure.

机译：犬肥厚衰竭的心室肌细胞中cGMP和cAMP的相互作用减少。

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Baseline function and signal transduction are depressed in hearts with hypertrophic failure. We tested the hypothesis that the effects of cGMP and its interaction with cAMP would be reduced in cardiac myocytes from hypertrophic failing hearts. Ventricular myocytes were isolated from control dogs, dogs with aortic valve stenosis hypertrophy, and dogs with pacing hypertrophic failure. Myocyte function was measured using a video edge detector. Cell contraction data were obtained at baseline, with 8-bromo-cGMP (10(-7), 10(-6), and 10(-5) M), with erythro-9-(2-hydroxy-3-nonyl)adenine [EHNA; a cAMP phosphodiesterase (PDE(2)) inhibitor] plus 8-bromo-cGMP, or milrinone (a PDE(3) inhibitor) plus 8-bromo-cGMP. Baseline percent shortening and maximal rates of shortening (R(max)) and relaxation were slightly reduced in hypertrophic myocytes and were significantly lower in failing myocytes (R(max): control dogs, 95.3 +/- 17.3; hypertrophy dogs, 88.2 +/- 5.5; failure dogs, 53.2 +/- 6.4 mum/s). 8-Bromo-cGMP dose dependently reduced myocyte function in all groups. However, EHNA (10(-6) M) and milrinone (10(-6) M) significantly reduced the negative effects of cGMP on cell contractility in control and hypertrophy but not in failing myocytes (R(max) for control dogs: cGMP, -46%; +EHNA, -21%; +milrinone, -19%; for hypertrophy dogs: cGMP, -40%; +EHNA, -13%; +milrinone, -20%; for failure dogs: cGMP, -40%; +EHNA, -29%; +milrinone, -32%). Both combinations of EHNA-cGMP and milrinone-cGMP significantly increased intracellular cAMP in control, hypertrophic, and failing myocytes. These data indicated that the cGMP signaling pathway was preserved in hypertrophic failing cardiac myocytes. However, the interaction of cGMP with the cAMP signaling pathway was impaired in these failing myocytes.
机译：肥厚衰竭心脏的基线功能和信号转导降低。我们测试了以下假设：在肥厚性衰竭心脏的心肌细胞中，cGMP的作用及其与cAMP的相互作用将降低。从对照犬，主动脉瓣狭窄肥大的犬和起搏肥大性衰竭的犬中分离出心室肌细胞。使用视频边缘检测器测量肌细胞功能。在基线时使用8-bromo-cGMP（10（-7），10（-6）和10（-5）M），在erythro-9-（2-hydroxy-3-nonyl）中获得细胞收缩数据腺嘌呤[EHNA; cAMP磷酸二酯酶（PDE（2））抑制剂]加8-溴cGMP，或米力农（PDE（3）抑制剂）加8-溴cGMP。肥大性心肌细胞的基线缩短率和最大缩短率（R（max））和松弛率略有降低，而衰竭的心肌细胞则明显降低（R（max）：对照犬，95.3 +/- 17.3;肥大犬，88.2 + / -5.5;失败犬，53.2 +/- 6.4 mum / s）。在所有组中，8-Bromo-cGMP剂量依赖性地降低了肌细胞功能。但是，EHNA（10（-6）M）和米力农（10（-6）M）显着降低了cGMP对对照和肥大细胞收缩性的负面影响，但对衰弱的心肌细胞却没有影响（R（max）对对照犬：cGMP ，-46％; + EHNA，-21％; +米力农，-19％;肥大犬：cGMP，-40％; + EHNA，-13％; +米力农，-20％;衰竭狗：cGMP，- 40％; + EHNA，-29％; +米力农，-32％）。 EHNA-cGMP和米力农-cGMP的两种组合均可显着增加对照，肥大性和衰竭性心肌细胞的细胞内cAMP。这些数据表明，cGMP信号通路在肥大性衰竭的心肌细胞中得以保留。但是，在这些衰竭的心肌细胞中，cGMP与cAMP信号通路的相互作用受到损害。

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