NDLI: Mechanisms underlying spontaneous constrictions of postcapillary venules in the rat stomach

Content Provider	Springer Nature Link
Author	Mitsui, Retsu Hashitani, Hikaru
Copyright Year	2015
Abstract	Postcapillary venules (PCVs) play a critical role in regulating capillary hydrostatic pressure, but their contractile mechanisms are not well understood. We examined the properties of spontaneous vasomotion and corresponding Ca2+ transients in gastric PCV. In the rat gastric submucosa, changes in PCV diameter and intracellular Ca2+ dynamics were visualised by video tracking system and fluorescent Ca2+ imaging, respectively, while PCV morphology was examined by immunohistochemistry. Stellate-shaped PCV mural cells expressing α-smooth muscle actin exhibited synchronised spontaneous Ca2+ transients to develop vasomotion which was abolished by nifedipine (1 μM), cyclopiazonic acid (10 μM), or Ca2+-activated Cl− channel inhibitors (100 μM niflumic acid, 1 μM T16Ainh-A01). A gap junction blocker (3 μM carbenoxolone) disrupted the synchrony of spontaneous Ca2+ transients amongst PCV mural cells and attenuated spontaneous vasomotion. Low chloride solution ([Cl−]0 = 12.4 mM) also disrupted the synchrony of spontaneous Ca2+ transients and abolished vasomotion. Na+-K+-Cl− co-transporter inhibitors (10 μM bumetanide, 30 μM furosemide) suppressed spontaneous Ca2+ transients and vasoconstrictions. A phosphodiesterase type 5 (PDE5) inhibitor (1 μM tadalafil) disrupted the spontaneous Ca2+ transient synchrony and abolished vasomotion in a nitric oxide (NO)-dependent manner. Thus, gastric PCVs exhibit spontaneous vasomotion, resulting from synchronised spontaneous Ca2+ transients within a network of stellate-shaped PCV mural cells. An active Cl− accumulation partly via Na+-K+-Cl− co-transport appears to be fundamental in maintaining depolarisation upon the opening of Ca2+-activated Cl− channels that triggers Ca2+ influx via voltage-dependent L-type Ca2+ channels. Basal PDE5 activity may continuously counteract vaso-relaxing effects of endothelial NO to maintain spontaneous vasomotion.
Starting Page	279
Ending Page	291
Page Count	13
File Format	PDF
ISSN	00316768
Journal	Pflügers Archiv
Volume Number	468
Issue Number	2
e-ISSN	14322013
Language	English
Publisher	Springer Berlin Heidelberg
Publisher Date	2015-11-04
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Microvasculature Contraction Smooth muscle Pericyte Rhythmicity Human Physiology
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Clinical Biochemistry

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