Potassium conductance and oscillatory contractions in tail arteries from genetically hypertensive rats

Abstract

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 (E_m) 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 (gK_Ca) 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 E_m. The channel-specific toxins apamin (4 x 10^-7mol/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^-4mmol), quinidine (5.8 x 1O^-5 mmol) and elevation of extracellular potassium (20mmol/l). Em recordings show that both potassium and barium convert bursting activity into tonic firing. Only 20mmol/l 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. Norepinephrineinduced electrical activity is diminished in the presence of quinidine. These results suggest that potassium conductance plays an important role in controlling E_m, electrical spiking and therefore oscillatory contractile activity in response to norepinephrine in the tail arteries of SHR-SP. However, no clear association between potassium conductance and the relaxation phase of the oscillations could be established. Since contractile activity was not inhibited by apamin or charybdotoxin, it is concluded that the cellular event which terminates the contractile phase of an oscillation (and also terminates spike activity) is not a toxin-sensitive gK_Ca.