腎素-血管緊張素系統(tǒng)（renin-angiotensin system, RAS）是影響血管平滑肌細(xì)胞張力的重要因素。RAS主要活性物質(zhì)血管緊張素Ⅱ （angiotensin Ⅱ, Ang Ⅱ）可通過激活血管緊張素Ⅱ-1型受體（angiotensin Ⅱ type 1 receptor, AT1R）升高胞內(nèi)Ca²⁺濃度,收縮平滑肌細(xì)胞。大電導(dǎo)鈣激活鉀(large-conductance Ca²⁺-and voltage-activated potassium, BK)通道是血管平滑肌細(xì)胞中分布最廣、表達最多的鉀離子通道,在維持細(xì)胞膜電位和胞內(nèi)鉀鈣平衡中發(fā)揮重要作用。血管平滑肌細(xì)胞上的BK通道主要包含α與β1兩種亞基。其中功能亞基BKα上分布有膜電位及Ca²⁺感受器。因此當(dāng)膜電位或細(xì)胞內(nèi)Ca²⁺濃度升高時會反饋性引起B(yǎng)K通道開放。然而,越來越多的研究顯示,盡管Ang Ⅱ可升高胞內(nèi)Ca²⁺濃度,但卻通過激活PKC通路、促進AT1R與BKα通道形成的異源二聚體內(nèi)吞、加快α與β1亞基解... 

【文章來源】：生理學(xué)報. 2019,71(02)北大核心CSCD

【文章頁數(shù)】：9 頁

【文章目錄】：
1 Introduction
2 The structure and function of the BK channel
3 The inhibitory effect of Ang II on the BK channel in VSMCs
    3.1 The direct or indirect inhibitory effect of PKC
    3.2 Increased endocytosis and degradation of the BK channel
    3.3 Down-regulation of BKβ1 subunit
4 The activating effect of Ang II on the BK channel in VSMCs
    4.1 The alternative splices of BKαsubunit
    4.2 The involvement of AT2 receptor (AT2R)
    4.3 The term of Ca2+in activating the BK channel
5 Conclusion and prospect



本文編號：3169505