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1 Departamento de Ciencias Fisiológicas, Pontificia Universidad Católica de Chile, Santiago, Chile
2 Institute of Biomedical Science, Academia Sinica, Nankang, Taipei, Taiwan - Republic of China
3 Howard Hughes Medical Inst, Univ of Iowa College of Med, Iowa City, Iowa, United States
4 Department of Molecular Physiology and Biological Physics, University of Virginia, Charlottesville, Virginia, United States
5 Charlottesville, Virginia, United States; Department of Molecular Physiology and Biological Physics, University of Virginia, Charlottesville, Virginia, United States
* To whom correspondence should be addressed. E-mail: brd{at}virginia.edu.
In the microcirculation, longitudinal conduction of vasomotor responses provides an essential means of coordinating flow distribution among vessels in a complex network. Spread of current along the vessel axis can display a regenerative component, which leads to propagation of vasomotor signals over many millimeters; the ionic basis for the regenerative response is unknown. We examined the responses to 10s of focal electrical stimulation (30Hz, 2ms, 30V) of mouse cremasteric arterioles to test the hypothesis that voltage-dependent Na+ (Nav) and Ca++ channels can be activated in long-distance signaling in micro-vessels. Electrical stimulation evoked a vasoconstriction at the site of stimulation and a spreading, non-decremental conducted dilation. Endothelial damage (air bubble) blocked the conduction of the vasodilation, indicating an involvement of the endothelium. The Nav blocker, bupivicaine also blocked conduction and tetrodotoxin attenuated it. The Nav activator, veratridine, induced an endothelium-dependent dilation. The Nav isoforms Nav1.2, Nav1.6 and Nav1.9 were detected in the endothelial cells of cremasteric arterioles by immunocytochemistry. These findings are consistent with the involvement of Nav channels in the conducted response. BAPTA buffering of endothelial cell Ca++ delayed and reduced the conducted dilation, which was almost eliminated by Ni++, amiloride, or deletion of 
1H T-type Ca++ channels (Cav3.2). Blockade of endothelial nitric oxide synthase (eNOS) or Ca++-activated K+ channels (KCa) also inhibited the conducted vasodilation. Our findings indicate that an electrically induced signal can propagate along the vessel axis via the endothelium and can induce sequential activation of Nav and Cav3.2. The resultant Ca++ influx activates both eNOS and KCa, triggering vasodilation.
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