title: Functional properties of submucosal venules in the rat stomach.
abstract: Venules in the stomach may have intrinsic properties for maintaining active microcirculation drainage even during gastric filling. Properties of spontaneous and nerve-mediated activity of submucosal venules in the rat stomach were investigated. Changes in vasodiameter and intracellular Ca(2+) in venular smooth muscle cells (SMCs) were monitored by video tracking and Fluo-8 Ca(2+) imaging, respectively. Venular SMCs developed synchronous spontaneous Ca(2+) transients and corresponding rhythmic constrictions of the venules. Nominally Ca(2+)-free solution or an L-type Ca(2+) channel blocker (1 μM nifedipine) disrupted the Ca(2+) transient synchrony and abolished spontaneous constrictions. Spontaneous constrictions were also prevented by inhibitors of sarcoplasmic reticulum Ca(2+)-ATPase (10 μM cyclopiazonic acid (CPA)), IP3 receptors (100 μM 2-APB) or Ca(2+)-activated Cl(-) channels (100 μM niflumic acid). Transmural nerve stimulation (TNS) induced a long-lasting venular constriction that was abolished by α-adrenoceptor antagonist (1 μM phentolamine), while TNS evoked a sympathetic transient constriction of arterioles that was abolished by a combination of phentolamine and a P2 purinoceptor antagonist (10 μM pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS)). Consistently, P2X1 purinoceptor immunoreactivity was detected in arteriolar but not venular SMCs. Primary afferent nerve stimulation (300 nM capsaicin) caused a venular dilatation by releasing calcitonin gene-related peptide. Thus, Ca(2+) release from the sarcoplasmic reticulum may play a fundamental role in the generation of spontaneous Ca(2+) transients, while electrical coupling amongst venular SMCs via L-type Ca(2+) channel activation appears to be critical for Ca(2+) transient synchrony as well as spontaneous contractions. Sympathetic venular constrictions appear to be exclusively mediated by noradrenaline due to the lack of P2X1 receptor in venular SMCs.
authors: Department of Cell Physiology, Nagoya City University Graduate School of Medical Sciences, 1, Kawasumi, Mizuho-cho, Mizuho-Ku, Nagoya, 467-8601, Japan, mitsui@med.nagoya-cu.ac.jp.
authors: Retsu
authors: R
authors: Mitsui
authors: Hikaru
authors: H
authors: Hashitani
mesh_terms: D001896:Boron Compounds / Q000494:pharmacology; D015740:Calcitonin Gene-Related Peptide / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020013:Calcium Signaling; D002211:Capsaicin / Q000494:pharmacology; D018118:Chloride Channels / Q000037:antagonists & inhibitors; D007211:Indoles / Q000494:pharmacology; D053496:Inositol 1,4,5-Trisphosphate Receptors / Q000037:antagonists & inhibitors; D007413:Intestinal Mucosa / Q000098:blood supply*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D009543:Nifedipine / Q000494:pharmacology; D009544:Niflumic Acid / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D011732:Pyridoxal Phosphate / Q000031:analogs & derivatives / Q000494:pharmacology; D013270:Stomach / Q000098:blood supply*; D014664:Vasodilation; D014665:Vasodilator Agents / Q000494:pharmacology; D014699:Venules / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*
chemical_list: C538758:2-aminoethyl diphenylborinate; D001896:Boron Compounds; D002121:Calcium Channel Blockers; D018118:Chloride Channels; D007211:Indoles; D053496:Inositol 1,4,5-Trisphosphate Receptors; D014665:Vasodilator Agents; C077792:pyridoxal phosphate-6-azophenyl-2',4'-disulfonic acid; D009544:Niflumic Acid; D011732:Pyridoxal Phosphate; D009543:Nifedipine; D015740:Calcitonin Gene-Related Peptide; D002211:Capsaicin; C000543:cyclopiazonic acid; D010646:Phentolamine