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1 Division of Renal and Cardiovascular Research, Department of Medical Physiology, The Panum Institute, University of Copenhagen, DK-2200 Copenhagen; and 2 Department of Physiology and Pharmacology, Odense University, DK-5000 Odense, Denmark
The purpose of the present study was to
investigate the conducted Ca2+ response to local electrical
stimulation in isolated rat interlobular arteries. Interlobular
arteries were isolated from young Sprague-Dawley rats, loaded with fura
2, and attached to pipettes in a chamber on an inverted microscope.
Local electrical pulse stimulation (200 ms, 100 V) was administered by
means of an NaCl-filled microelectrode (0.7-1 M
) juxtaposed to
one end of the vessel. Intracellular Ca2+ concentration
([Ca2+]i) was measured with an image system
at a site ~500 µm from the location of the electrode. The
expression of mRNA for pore-forming units CaV3.1 and
CaV3.2 of voltage-sensitive T-type channels was investigated by using RT-PCR. Current stimulation elicited a conducted [Ca2+]i response. A positive electrode
(relative to ground) increased [Ca2+]i to
145 ± 7% of baseline, whereas the response was absent when the
electrode was negative. This response was not dependent on perivascular
nerves, because the conducted response was unaffected by TTX (1 µM).
The conducted [Ca2+]i response was abolished
by an ambient Ca2+ free solution and blunted by nifedipine
(1 µM). Rat interlobular arteries exhibited conducted
[Ca2+]i response to current stimulation. This
response was dependent on Ca2+ entry. L-type
Ca2+ channels may play a role in this process.
microcirculation; vascular smooth muscle; hemodynamics; nifedipine; mibefradil; calcium channels
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