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.