Tail arteries isolated from the stroke-prone substrain of the spontaneously hypertensive rat (SHR-SP) exhibit oscillatory contractile responses to norepinephrine. Simultaneous recording of force generation and membrane potential (Em) has previously demonstrated that the contractile phase of these oscillations is associated with bursts of calcium-dependent action potentials. The smooth muscle cells are electrically quiescent during the relaxation phase of the oscillations. The present studies were designed to test the hypothesis that this quiescent period results from the stimulation of a calcium-activated potassium conductance (gKCa) in the cells responsible for triggering the bursting activity. Isolated tail artery strips from SHR-SP and Wistar-Kyoto rats (WKY) were prepared for measurement of isometric force generation or for simultaneous recording of force and Em. The channel-specific toxins apamin (4 x 10(-7) mol/l) and charybdotoxin (4.7 x 10(-8) did not alter the oscillatory pattern of contraction in response to norepinephrine. Oscillations were converted to sustained contraction by barium (10(-4) mmol), quinidine (5.8 x 10(-5) mmol) and elevation of extracellular potassium (20 mmol/l). Em recordings show that both potassium and barium convert bursting activity into tonic firing. Only 20 mmol/k+ caused significant depolarization in addition to that produced by norepinephrine. In contrast, quinidine appears to alter oscillatory behavior by interfering with calcium-spike generation. Norepinephrine-induced electrical activity is diminished in the presence of quinidine. These results suggest that potassium conductance plays an important role in controlling Em, electrical spiking and therefore oscillatory contractile activity in response to norepinephrine in the tail arteries of SHR-SP.(ABSTRACT TRUNCATED AT 250 WORDS)