Spontaneous activity and regulatory mechanisms of rectal microvessels

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K19361
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Gastroenterology
• Research Institution: Nagoya City University
• Principal Investigator: Mitsui Retsu 名古屋市立大学, 大学院医学研究科, 講師 (90434092)
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: 細動脈 / 平滑筋 / 周皮細胞 / カルシウムイメージング / 自発活動 / Cl-チャネル / 電位依存性Ca2+チャネル / ギャップ結合

Outline of Final Research Achievements

The mural cells (vascular smooth muscle cells and pericytes) of rectal arterioles periodically exhibited synchronous, spontaneous rise in intracellular Ca2+ concentration. These spontaneous Ca2+ transients depended on Ca2+ release from endoplasmic reticulum Ca2+ store and subsequent Ca2+-activated Cl- channel opening-mediated Cl- efflux which are expected to cause membrane depolarisation. The depolarisation appeared to be large enough to electrically couple the mural cells connected via gap junctions. Subsequent Ca2+ influxes through T-type (TVDCCs) and L-type (LVDCCs) voltage-dependent Ca2+ channels underlay ‘synchronous’ spontaneous Ca2+ transients among the mural cells. The openings of TVDCCs and LVDCCs increased Ca2+ transient frequency and duration, respectively. The synchronous spontaneous Ca2+ transients in the mural cells may underlie the spontaneous constrictions of arterioles to prevent the rectum from ischemic damage during the prolonged wall distension by faecal pellets.

Free Research Field

生理学・形態学