Ionic mechanisms in spontaneous vasomotion of the rat basilar artery in vivo.

1. The goal of this study was to examine ionic mechanisms that modulate spontaneous rhythmic changes in vascular calibre or 'vasomotion' in the basilar artery in vivo. 2. Diameter of the basilar artery was measured through a craniotomy in anaesthetized rats under control conditions and during topical application of antagonists or alteration in the ionic composition of artificial cerebrospinal fluid (CSF). 3. Both Ca2(+)-free CSF and the Ca2+ channel blocker, nimodipine, produced moderate dilatation of the basilar artery and abolished vasomotion. Increasing the concentration of Ca2+ in CSF from 1.7 to 5.0 mM did not affect the frequency of vasomotion, although the amplitude was increased slightly. 4. Both K(+)-free CSF and ouabain produced mild to moderate vasoconstriction and abolished vasomotion. In contrast, increasing the concentration of K+ in CSF produced vasodilatation of the basilar artery and decreased or abolished vasomotion depending on the degree of vasodilatation. 5. Tetrodotoxin had no effect on vasomotion. 6. These results suggest that vasomotion of the basilar artery in vivo is dependent on extracellular Ca2+ and K+, and on the activity of Na(+)-K(+)-ATPase, and not dependent on Na+ channel.