Moncek Fedor, Aguilera Greti, Jezova Daniela
Institute of Experimental Endocrinology, Slovak Academy of Sciences, Vlarska 3, 83306 Bratislava, Slovakia.
J Neuroimmunol. 2003 Sep;142(1-2):86-92. doi: 10.1016/s0165-5728(03)00268-6.
We have tested the hypothesis that chronic inflammatory stress results in changes in sympathoadrenal and renin-angiotensin-aldosterone responses to novel stressors. Repeated treatment of rats with increasing doses of lipopolysaccharide (LPS) resulted in a decrease of plasma adrenaline and aldosterone as well as in renin activity (angiotensin I) responses compared to those after acute administration. Repeated LPS administration was associated with decreased plasma aldosterone responses to a different stressor (immobilization) in spite of preserved or even elevated responses of plasma renin activity and catecholamines. These alterations may contribute to the development of cardiovascular complications during chronic inflammatory states.
慢性炎症应激会导致交感肾上腺系统以及肾素 - 血管紧张素 - 醛固酮系统对新的应激源的反应发生变化。与急性给药后相比,用递增剂量的脂多糖(LPS)反复处理大鼠会导致血浆肾上腺素和醛固酮减少,以及肾素活性(血管紧张素I)反应降低。尽管血浆肾素活性和儿茶酚胺的反应保持不变甚至升高,但反复给予LPS与血浆醛固酮对另一种应激源(固定)的反应降低有关。这些改变可能有助于慢性炎症状态下心血管并发症的发展。