Chemoreflex dysfunction in heart failure cellular mechanisms
作者单位：Department of Cellular and Integrative PhysiologyUniversity of Nebraska Medical CenterOmahaNEUSA 68198-5800
会议名称：《2008北京国际生理科学学术大会》
会议日期：2008年
学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学]
关 键 词：caiotid body heart failure angiotensinⅡ nitric oxide K channels
摘 要：Alterations in carotid body(CB)function can be a contributing factor to the pathophysiology of various cardiopulmonary diseases,including hypertension and heart failure(HF).We have demonstrated that the CB chemoreflex is enhanced in *** sensitization contributes to tonic sympathetic hyperactivity in HF,which exacerbates morbidity and mortality of the *** of CB reflex function arises in large part from an increased activity of CB chemoreceptors under both normoxic and hypoxic *** analysis of CB function in HF rabbits and rats suggests that multiple cellular mechanisms are engaged to alter the redox state at the level of the CB type 1(glomus)cells to favour enhanced ROS inhibition of O sensitive voltage gated K currents(I.A prooxidant state is induced through an increase in local AngiotensinⅡ(AngⅡ)production via downregulation of ACE-2 and upregulation of ACE-1 within the ***Ⅱ-activated ROS production via NADPH-oxidase is enhanced and contributes to inhibition of I in CB glomus cells in *** pro-oxidant state is reinforced by a downregulation of SOD-1 and SOD-2 in glomus *** also suggests that AngⅡenhances superoxide production from mitochondria in CB glomus ***,both nitric oxide synthase(NOS-1 and NOS-3)and heme-oxyge- nase(HO-2)are downregulated in the CB in HF,with loss of NO- and CO-activation of I in glomus *** associated with HF that may play a role in this plasticity of the CB will be discussed.