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

Abstract

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 (α1C-subunit), whereas mRNA coding for T-type subunits was found (α1G- and α1H-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.