学术报告：小动脉的传导性抑制/扩张：细胞机制及其数学模型

报告题目：小动脉的传导性抑制/扩张：细胞机制及其数学模型

报告人：蒋志根, Associate Professor, Oregon Health & Science University, Portland, U.S.A.

报告时间：2009年10月12日上午10时

报告地点：独墅湖校区医学楼403-3119室

报告人简介：

蒋志根博士长期从事神经系统和心血管系统细胞电生理学和功能解剖学的研究。揣长于用膜片钳技术结合分子生物学等多种方法，研究受体、离子通道和第二信使等突触传递过程。近年来着重研究内耳血管结构的细胞电生理，曾多次获得NIH资助。他作为Principal Investigator在J Physiol、Hear Res以及 J Pharmacol Exp Ther等著名刊物上发表论文多篇。

Abstract

Focal hyperpolarization and dilation induced by vasodilators such as acetylcholine (ACh) may conduct along the arterial axis with little or no decay. Such conductive dilation contributes to blood flow control in vascular resistance networks but the underlying mechanism remains to be clarified. Using intracellular, whole-cell recording and labeling techniques, and mathematic modeling analysis, we explored cellular/channel mechanisms of such conductive inhibition in guinea pig cochlear spiral modiolar artery (SMA), and found:

The arterial cells express abundant inward rectifier K⁺-channels (Kir) which is critical for the regenerative shift of the resting potentials while other conductances collectively determine the voltage level that permit or prevent the regeneration. ACh activates intermediate conductance Ca ²⁺-activated K⁺-channels (IK) and causes hyperpolarization in the endothelial cells. The hyperpolarization spread to the muscular layer via gap junctions and disinhibits the Kir. The intercellular electro-coupling and the positive feedback in the loop of hyperpolarization→Kir disinhibition→further hyperpolarization form the mechanism for the conductive inhibition and dilation. Such conductive dilation amplifies the effect of focal dilatory factor, e.g., K⁺ elevation, thus provides a fast and sensitive blood flow regulation to accommodate the surge of energy consumption in organs, such as the inner ear and skeleton muscles. The conductive dilation may also underlie some forms of headache.