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Am J Physiol Heart Circ Physiol 280: H582-H590, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 2, H582-H590, February 2001

Conducted vasoconstriction in rat mesenteric arterioles: role for dihydropyridine-insensitive Ca2+ channels

Finn Gustafsson1, Ditte Andreasen2, Max Salomonsson1, Boye L. Jensen2, and Niels-Henrik Holstein-Rathlou1

1 Division of Renal and Cardiovascular Research, Department of Medical Physiology, Panum Institute, University of Copenhagen, DK-2200 Copenhagen; and 2 Department of Physiology and Pharmacology, Odense University, DK-5000 Odense, Denmark

The aim of this study was to evaluate the role of voltage-operated Ca2+ channels in the initiation and conduction of vasoconstrictor responses to local micropipette electrical stimulation of rat mesenteric arterioles (28 ± 1 µm, n = 79) in vivo. Local and conducted (600 µm upstream from the pipette) vasoconstriction was not blocked by TTX (1 µmol/l, n = 5), nifedipine, or nimodipine (10 µmol/l, n = 9). Increasing the K+ concentration of the superfusate to 75 mmol/l did not evoke vasoconstriction, but this depolarizing stimulus reversibly abolished vasoconstrictor responses to current stimulation (n = 7). Addition of the T-type Ca2+ antagonist mibefradil (10 µmol/l, n = 6) to the superfusate reversibly blocked local and conducted vasoconstriction to current stimulation. With the use of RT-PCR techniques, it was demonstrated that rat mesenteric arterioles <40 µm do not express mRNA for L-type Ca2+ channels (alpha 1C-subunit), whereas mRNA coding for T-type subunits was found (alpha 1G- and alpha 1H-subunits). The data indicate that L-type Ca2+ channels are absent from rat mesenteric arterioles (<40 µm). Rather, the vasoconstrictor responses appear to rely on other types of voltage-gated, dihydropyridine-insensitive Ca2+ channels, possibly of the T-type.

L-type Ca2+ channels; T-type Ca2+ channels; mibefradil; Ca2+ channel antagonists; RT-PCR


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