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; 3nM) 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.