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Department of Physiology, Semmelweis University of Medicine, Budapest, Hungary.

1. We examined Ca2+ influx mechanisms using the whole-cell patch-clamp technique in primary cultures of rat glomerulosa cells. 2. Depolarization of the plasma membrane, as studied by a stepwise or ramp depolarization technique, activated low-threshold, transient (T-type) and high-threshold, long-lasting (L-type) voltage-dependent calcium channels (VDCCs). 3. Extracellular K+ activated an inward current (Ig1), even in voltage-clamped cells. This phenomenon was observed within the physiological concentration range, beginning at 4.6 mM K+o (as opposed to the control level of 3.6 mM K+o). Increased cell conductance and increased background noise indicated that Ig1 is evoked by enhanced channel activity. Potassium induced no outward current in the voltage range examined (-120 to +60 mV). 4. When non-permeable anions were present only in the pipette and Na+ and Mg2+ were omitted from the bath, K+ still activated the current. Ig1 was blocked by 100 microM cadmium but was insensitive to 2 microM nifedipine or to 300 microM Ni2+. 5. In fluorimetric studies elevation of the cytoplasmic Ca2+ concentration in response to K+ (5.6-13.6 mM) was reduced only partially when VDCCs were blocked with Ni2+ (200 microM) and nifedipine (2 microM). 6. Elevation of the K+ concentration shifted the threshold potential of the T-type calcium channel in the negative direction. 7. In summary, K+ as a ligand activates Ca(2+)-permeable channels in rat glomerulosa cells. This current may contribute to the development of Ca2+ signals in response to stimulation with K+ in the physiological range. The reduction of the activation threshold of the T-type current by K+ may also be of physiological significance.

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