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首页> 外文期刊>American Journal of Physiology >Angiotensin II modulates catecholamine release into interstitial fluid of canine myocardium in vivo.
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Angiotensin II modulates catecholamine release into interstitial fluid of canine myocardium in vivo.

机译：血管紧张素II在体内调节儿茶酚胺释放到犬心肌的组织液中。

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This study tested the hypothesis that exogenous infusion of angiotensin II (ANG II) leads to the release of catecholamines [norepinephrine (NE) and epinephrine (EPI)] into the cardiac interstitial fluid (ISF) space of dogs with adrenals intact (AI) (n = 7) and with adrenals clamped (AC) (n = 5). LV ISF samples were collected at 3-min intervals during administration of ANG II (100 microM ANG II at 1 ml/min for 10 min) to right atrial neurons via their local arterial blood supply and during electrical stimulation of the stellate ganglia of open-chest anesthetized dogs. In AI dogs, ANG II caused ISF NE to increase fivefold (P < 0.05) without a significant increase in coronary sinus (CS) NE. Electrical stimulation (5 ms, 4 Hz, 8-14 V, and 10 min) of the stellate ganglia caused a similar increase in ISF NE (P < 0.05), accompanied by a sevenfold increase in CS NE (P < 0.05). ISF EPI increased greater than sixfold during ANG II infusion (P < 0.05) and during stellate stimulation. However, during ANG II infusions, aorta plasma EPI levels increased fourfold in AI dogs, whereas in AC dogs, CS NE and EPI levels were unaffected during ANG II infusions. Nevertheless, baseline ISF NE and EPI did not differ and increased to a similar extent during ANG II infusions in AI versus AC dogs. Thus exogenously administered ANG II increases the amount of NE liberated into the ISF independent of the adrenal contribution, the amount matching that induced by electrical stimulation of all cardiac sympathetic efferent neurons. In contrast, NE spillover into the CS occurred only during electrical stimulation of stellate ganglia. NE release and uptake mechanisms within the myocardium are differently affected, depending on how the final common pathway of the sympathetic efferent nervous system is modified.
机译：这项研究检验了以下假设：外源性注射血管紧张素II（ANG II）导致儿茶酚胺[去甲肾上腺素（NE）和肾上腺素（EPI）]释放到具有肾上腺完整（AI）的犬的心脏间质液（ISF）空间中（ n = 7），并夹有肾上腺（AC）（n = 5）。左室ISF样本是在通过局部动脉血供向右心房神经元施用ANG II（100 microM ANG II，以1 ml / min的速度持续10分钟）和电刺激开放式星状神经节期间，每隔3分钟收集一次胸部麻醉的狗。在AI犬中，ANG II导致ISF NE增加五倍（P <0.05），而冠状窦（CS）NE没有明显增加。星状神经节的电刺激（5 ms，4 Hz，8-14 V和10分钟）引起了类似的ISF NE增加（P <0.05），同时CS NE增加了七倍（P <0.05）。在ANG II输注过程中和星状刺激过程中，ISF EPI增加了六倍以上（P <0.05）。然而，在ANG II输注期间，AI狗的主动脉血浆EPI水平增加了四倍，而在AC犬中，在ANG II输注期间CS NE和EPI水平未受影响。不过，在AI和AC狗中进行ANG II输注期间，基线ISF NE和EPI没有差异，并以相似的程度增加。因此，外源给予的ANG II增加了独立于肾上腺贡献而释放到ISF中的NE的量，该量与通过电刺激所有心脏交感神经传出神经元诱导的量相匹配。相反，NE仅在星状神经节的电刺激过程中才溢出到CS中。心肌内NE的释放和摄取机制受到不同的影响，具体取决于交感神经传出神经系统的最终通用途径是如何被修饰的。

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