| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| 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.
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