Properties of calcium channels in guinea‐pig gastric myocytes.

Abstract

SUMMARY1. The inward membrane current in enzymatically dispersed guinea-pig gastric myocytes was studied using whole-cell voltage clamp technique.2. Only one inward membrane current was found in gastric myocytes which was identified as the Ca2+ current based on its inhibition by Ni2+, Cd2+ and Co2+, its dependence on [Ca2 ]0, and its insensitivity to variations of [Na+]O.3. Ca2+ current activated at -20 mV, peaked around + 10 mV and was markedly enhanced when the holding potential was increased from -40 to -90 mV. The enhancement of ICa at negative holding potentials did not alter the activation threshold Of Ica-When Ba2+ was substituted for Ca2+, IBa was similarly enhanced at more negative potentials.4. In cells where internal Ca2+ was buffered with 10 mM-EGTA, the time course of inactivation was fitted with two exponentials, with time constants: rT = 53.4+1841 ms and Ts = 175-2 + 46-1 ms. When Ba2+ was the charge carrier through the channel, the time course of inactivation could be fitted often by only one exponential which approximated TS for inactivation of ICa. The [H+]. appeared to differentially affect peak and maintained components of ICa. At pH < 6 5, the maintained component of 'Ca was suppressed more than the peak component indicating possible time-and voltage-dependent inhibition of ICa by protons. D. A. KATZKA AND M. MORAD 8. Nifedipine, D600 and diltiazem inhibited ICa in a voltage-dependent manner. The order of potency for inhibition of peak ICa was nifedipine t D600 > diltiazem. Diltiazem, unlike the other two drugs, enhanced the inactivation of ICa' even when peak ICa' was not affected suggesting either a time-and voltage-dependent block of the open channel or possible existence of more than one population of Ca2+ channels with different drug sensitivities.9. At much lower concentration (100 nM) diltiazem enhanced the peak but not the maintained component of the Ca2+ current. A similar agonistic effect was also recorded for D600.10. The Ca2+ channel in the guinea-pig gastric myocyte is similar to Ca2+ channels of other tissues in its activation, ionic selectivity and inactivation. The inactivation of the Ca2+ channel is dependent both on voltage and [Ca2+]i. Although some of our data support the possible presence of more than one population of Ca2+ channels, we could provide definitive proof for only one channel type.

Cholinergic inhibition of Ca2+ current in guinea‐pig gastric and tracheal smooth muscle cells.

“…In summary, Ca2P currents recorded from gastric smooth muscle cells using the perforated patch technique were qualitatively similar to those described previously in gastric cells studied using conventional whole-cell recording (Katzka & Morad, 1989;Noack, Deitmer & Lammel, 1991;Sims, 1992b configurations, since we also record larger Ca2+ currents in guinea-pig gastric smooth muscle cells when using conventional whole-cell recording.…”

Ca2+ channel modulating effects of heparin in mammalian cardiac myocytes.

“…To test this possibility Ca2+ was replaced by Ba2+ as a charge carrier. EGTA (100 /M) was added to the Ba2+-containing Tyrode solution to bind possible contaminant Ca2+ concentrations (Katzka & Morad, 1991). Figure 7 shows that although the time course of inactivation of the Ca2+ channel was significantly slowed when Ba2+ was the charge carrier, the current through the channel was still suppressed by about 35 % in a manner quite similar to that observed in high EGTA-buffered cells (e.g.…”

Rabbit intestinal smooth muscle calcium current in solutions with physiological calcium concentration

“…The use of nifedipine as a straightforward probe for the presence of T-and L-type currents is, however, complicated by the fact that this drug accelerates Ca2`current decay even when a homogenous population of Ca2" channels was present (Inoue et al 1989), due perhaps to open-channel block, or preferential binding of dihydropyridine to inactivated channels (Bean, 1984;Gurney, Nerbonne & Lester, 1985). In addition, several studies have revealed that nifedipine and other Ca2 ' antagonists' sometimes increase the Ca2" current, especially at rather negative holding and test potentials (Kunze, Hamilton, Hawkes & Brown, 1987;Aaronson et al 1988;Katzka & Morad, 1989). In the present study, the shape and position on the voltage axis of the Ca2" current I-V relationship were not modified by this drug.…”