Abstract
The modulation of Na channels by the vasoactive peptide angiotensin II (AT II) has been studied in isolated ventricular cells of guinea pigs using the patch clamp technique. In cell-attached patches the maximal probability of the channel being open was increased in a concentration range between 0.05 and 1 μM, but decreased at higher concentrations. A maximal increase of 2.5 ± 0.86 was found at 1 μM AT II. The increase in the probability of the channel being open was due to a decrease in the number of nulls. In all affected cells ( n = 17) we observed a delayed inactivation after application of AT II at concentrations between 0.05 and 10 μM. At −30 mV, the time constant of inactivation increased from 1.1 ± 0.1 ms (controls) to 5.6 ± 1.6 ms (10 μM AT II). This effect was due to an increased number of openings per sweeps. No significant effect on the mean open time and the first latency were observed. However, due to pronounced bursting, the averaged closed time was significantly increased from 0.8 ± 0.1 ms to 1.3 ± 0.1 ms in the presence of 1 μM AT II at −30 mV. An effect of AT II on cardiac Na channels via protein kinase C is discussed.
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