Computer program for performing whole-cell voltage-clamp experiments.

This computer program was designed to be used instead of a stimulator and an oscilloscope in whole-cell voltage-clamp experiments. It runs on IBM XT-AT compatible computers under MS-DOS. The program uses drivers for specific ADC-DAC boards, which are stored in separate files. The driver to be used is loaded on start-up. Drivers for Labmaster TL-1 and CSY-10 are available and the driver for CED 1401 is now being developed. Stimulus waveforms of up to five consecutive pulses are supported. Data may be acquired from up to four input channels, using two ADC sampling rates. The acquired data are visualised on six plots which can be resized and moved independently on the screen in order to obtain a readable picture. A special mode for monitoring the giga-seal formation is supported. There are several data processing procedures, which can be used without interrupting the experiment, including I-V relationships, cursor measurements, addition and subtraction of obtained currents.

Cyclic GMP-induced activation of potassium currents by sarcoplasmic reticulum Ca2+ pump-dependent mechanism.

In voltage-clamped single smooth muscle cells from the circular layer of the guinea-pig gastric fundus NO-liberating substance or an analogue of cyclic 3, 5'-guanosine monophosphate (cGMP) increased or decreased the outward K+ current amplitudes depending on the Ca2+ buffering capacity of the intracellular medium. In a high EGTA-containing pipette solution dibutyryl-cGMP or sodium nitroprusside (SNP) attenuated both the fast and the late K+ current components. In pipette solution with lower Ca2+ -buffering capacity these drugs caused a sustained increase of K+ current amplitudes, which was effectively antagonized by thapsigargin, an inhibitor of Ca2+ -ATPase in the sarcoplasmic reticulum (SR). Our data suggest that, in gastric fundus smooth muscles, NO-liberating substances and cGMP analogues contribute to the activation of a Ca2+ -release mechanism from the cell bulk, i.e. the myoplasm surrounding the contractile filaments, towards the plasma membrane, crossing the SR Ca2+ -stores. Thus, a decreased intracellular free calcium concentration ([Ca2+]) is coupled with an elevation of subplasmalemmal calcium, which in turn causes cell membrane hyperpolarization. The latter is a consequence of the opening of tetraethylammonium-sensitive Ca2+ -activated K+ channels and leads to sustained smooth muscle relaxation, most characteristic for gastric fundus preparations.