SPONTANEOUS VASOMOTION IN HAMSTER-CHEEK POUCH ARTERIOLES IN VARYING EXPERIMENTAL CONDITIONS

The spontaneous rhythmic motor activity (vasomotion) of arterioles was studied in vivo in the hamster cheek pouch by means of intravital microscopy. In control conditions, arteriolar vasomotion was regularly present in healthy preparations, independent of anesthesia (pentobarbital sodium or alpha-chloralose), composition of the superfusate [tris(hydroxymethyl)aminomethane-buffered or N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-supported HCO3(-)-buffered saline solutions) or a combined nerve, alpha- and beta-receptor blockade. In arterioles with internal diameters between 13 and 52-mu-m, the vasomotion frequency (3-15 cycles/min) and amplitude (2-10-mu-m) were not significantly correlated to vessel size. The frequency and amplitude of the spontaneous arteriolar vasomotion could be modified by changes in the physical and chemical environment of the preparation. Thus, addition of pinacidil, a K+ channel activator, to the superfusate dose dependently decreased and finally suppressed vasomotion, in combination with an increase of the vessel diameter. These effects could be counteracted if glibenclamide (10(-6) M), a K+ channel blocker, was added to the superfusing solution. In the absence of any major changes in vessel diameter, vasomotion was also abolished by increasing the PO2 (from approximately 15 to 30 mmHg), varying the pH (from 7.40 to 7.22 or 7.65), and lowering the temperature to 15-degrees-C in the superfusion solution. The abolition of vasomotion observed because of increased PO2 and changes in pH could be reversed by addition of glibenclamide (10(-6) M) or tetraethylammonium chloride (TEA, 5 x 10(-3) M), another K+ channel blocker, to the superfusion solution; in the case of lowered temperature only glibenclamide was effective. The results support the hypothesis that, in the investigated vessels, vasomotion represents a myogenic activity sustained by a delicate balance between membrane currents among which K+ currents passing through TEA-, pinacidil-, and glibenclamide-sensitive membrane channels seem to play an important role.