Potassium-induced intermittent vasomotion in rat isolated pulmonary artery

A novel intermittent vasomotion induced by potassium in rat pulmonary artery was investigated with a view to characterize the ion channel mechanisms governing such secondary oscillatory activity. Isometric force was recorded from ring preparations of rat isolated pulmonary arteries incubated in a modified Krebs buffer containing K⁺ 15-18 mM and nitro-L-arginine methyl ester (10 µM). Tissues exhibited a stable pattern of on-off vasomotion consisting of intermittent contractile wave (ICW) activity with a periodicity of 7-8/hr and a rising phase of oscillatory ramping-up of contractile tone at 7 cycles/min. L-channel antagonists arrested (nicardipine; 3 nM) or retarded (verapamil, 30 nM) ICW activity with a concomitant wave asynchronization or decrease in amplitude. Mibefradil (30-100 nM) inhibited ICW ramping-up without affecting ICW period. Niflumic acid (1.0-3.0 µM) exerted dual actions on ICW amplitude but arrested ICW cycling at 10 µM. K⁺-channel blockers produced shortening of ICW period (4-aminopyridine, Ba²⁺ 30 µM; Cs⁺ 3.0-6.0 mM) and increase (tetraethylammonium; 1.0 mM) or decrease (Ba²⁺, 100 µM) in amplitude. Cyclopiazonic acid caused ICW asynchronization (0.3 µM) or cessation (1.0 µM) of ICW cycling. Fasudil retarded ramping-up contractile oscillations without changing ICW period. The inhibitory effects of nicardipine, niflumic acid and cyclopiazonic acid were partially surmounted by small additional increments in [K⁺](e). Our findings support the concept that a secondary vasomotive oscillator operates in rat pulmonary artery which enables the activity of the primary oscillator to be regulated in a cyclic manner via sarcolemmal L-type Ca²⁺ channels and an array of K conductances.