Local electric stimulation causes conducted calcium response in rat interlobular arteries.
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Local electric stimulation causes conducted calcium response in rat interlobular arteries. / Salomonsson, Max; Gustafsson, Finn; Andreasen, Ditte; Jensen, Boye L; Holstein-Rathlou, N.-H.
In: American Journal of Physiology - Renal Physiology, Vol. 283, No. 3, 2002, p. F473-80.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Local electric stimulation causes conducted calcium response in rat interlobular arteries.
AU - Salomonsson, Max
AU - Gustafsson, Finn
AU - Andreasen, Ditte
AU - Jensen, Boye L
AU - Holstein-Rathlou, N.-H.
N1 - Keywords: Animals; Arteries; Calcium; Calcium Channel Blockers; Calcium Channels; Calcium Channels, L-Type; Calcium Channels, T-Type; Electric Conductivity; Electric Stimulation; Mibefradil; Microelectrodes; RNA, Messenger; Rats; Reverse Transcriptase Polymerase Chain Reaction; Tetrodotoxin
PY - 2002
Y1 - 2002
N2 - The purpose of the present study was to investigate the conducted Ca(2+) 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(Omega)) juxtaposed to one end of the vessel. Intracellular Ca(2+) concentration ([Ca(2+)](i)) was measured with an image system at a site approximately 500 microm from the location of the electrode. The expression of mRNA for pore-forming units Ca(V)3.1 and Ca(V)3.2 of voltage-sensitive T-type channels was investigated by using RT-PCR. Current stimulation elicited a conducted [Ca(2+)](i) response. A positive electrode (relative to ground) increased [Ca(2+)](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 microM). The conducted [Ca(2+)](i) response was abolished by an ambient Ca(2+) free solution and blunted by nifedipine (1 microM). Rat interlobular arteries exhibited conducted [Ca(2+)](i) response to current stimulation. This response was dependent on Ca(2+) entry. L-type Ca(2+) channels may play a role in this process.
AB - The purpose of the present study was to investigate the conducted Ca(2+) 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(Omega)) juxtaposed to one end of the vessel. Intracellular Ca(2+) concentration ([Ca(2+)](i)) was measured with an image system at a site approximately 500 microm from the location of the electrode. The expression of mRNA for pore-forming units Ca(V)3.1 and Ca(V)3.2 of voltage-sensitive T-type channels was investigated by using RT-PCR. Current stimulation elicited a conducted [Ca(2+)](i) response. A positive electrode (relative to ground) increased [Ca(2+)](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 microM). The conducted [Ca(2+)](i) response was abolished by an ambient Ca(2+) free solution and blunted by nifedipine (1 microM). Rat interlobular arteries exhibited conducted [Ca(2+)](i) response to current stimulation. This response was dependent on Ca(2+) entry. L-type Ca(2+) channels may play a role in this process.
U2 - 10.1152/ajprenal.00247.2001
DO - 10.1152/ajprenal.00247.2001
M3 - Journal article
C2 - 12167598
VL - 283
SP - F473-80
JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology
JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology
SN - 1931-857X
IS - 3
ER -
ID: 8420389