Properties of synchronous spontaneous Ca2+ transients in the mural cells of rat rectal arterioles
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Synchrony of spontaneous Ca2+ transients among venular mural cells (smooth muscle cells and pericytes) in visceral organs relies on the intercellular spread of L-type voltage-dependent Ca2+ channel (LVDCC)-dependent depolarisations. However, the mechanisms underlying the synchrony of spontaneous Ca2+ transients between arteriolar mural cells are less understood. The spontaneous intracellular Ca2+ dynamics of arteriolar mural cells in the rat rectal submucosa were visualised by Cal-520 Ca2+ imaging to analyse their synchrony. The mural cells in fine arterioles that had a rounded cell body with several extended processes developed spontaneous ‘synchronous’ Ca2+ transients arising from Ca2+ released from sarcoendoplasmic reticulum Ca2+ stores. Gap junction blockers (3 μM carbenoxolone, 10 μM 18β-glycyrrhetinic acid), a Ca2+-activated Cl− channel (CaCC) blocker (100 μM 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid) or lowering extracellular Cl− concentration (from 134.4 to 12.4 mM) disrupted the synchrony of Ca2+ transients between arteriolar mural cells. Blockers of T-type voltage-dependent Ca2+ channels (TVDCCs, 1 μM mibefradil or ML218) or LVDCCs (1 μM nifedipine) reduced the Ca2+ transient frequency or their area under curve (AUC), respectively. However, neither TVDCC nor LVDCC blockers disrupted the synchrony of Ca2+ transients among arteriolar mural cells. This is in contrast with rectal venules in which nifedipine disrupted the synchrony of spontaneous Ca2+ transients. Thus, spontaneous transient depolarisations arising from the opening of CaCCs may effectively spread to neighbouring arteriolar mural cells via gap junctions to maintain the Ca2+ transient synchrony. Activation of TVDCCs appears to accelerate spontaneous Ca2+ transients, while LVDCCs predominantly contribute to the duration of Ca2+ transients.
KeywordsBlood vessel Microvasculature Smooth muscles Ca2+ signalling Intestine
α-Smooth muscle actin
Area under curve
Ca2+-activated Cl− channel
L-type voltage-dependent Ca2+ channel
NG2 chondroitin sulphate proteoglycan
Physiological salt solution
T-type voltage-dependent Ca2+ channel
The authors wish to thank Dr. Richard Lang (Monash University) for critical reading of the manuscript. The present study was partly supported by Grant-in-Aid for Young Scientists (B) (No. 26860521 and No. 16K19361) from Japan Society for Promotion of the Science (JSPS) to R.M., Grant-in-Aid for Challenging Exploratory Research (No. 26670705) from JSPS to H.H. and Grant-in-Aid from The Hori Sciences and Arts Foundation to R.M.
Compliance with ethical standards
The experimental protocols in the present study were approved by the animal experimentation ethics committee at Nagoya City University Graduate School of Medical Sciences.
Conflict of interest
The authors declare that they have no conflict of interest.
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