The membrane current evoked by histamine in isolated smooth muscle cells from rabbit basilar artery was investigated using the perforated-patch technique. When 10 μM histamine was applied in the bath at a holding potential of 60 mV, an inward current (79.2 ± 55.8 pA) was transiently activated. An outward current was additionally evoked by 10 μM histamine when the membrane was held at -40 mV or less negative potentials. The outward but not the inward current was completely blocked by 100 nM charybdotoxin. A higher concentration of histamine (30 μM) failed to produce the inward current (3.4 ± 4.8 pA) when Cl- concentration in the pipette was reduced. The apparent reversal potential of the inward current induced by histamine in physiological salt solution, in high-tetraethylammonium (TEA+) solution (bath), or in low-Cl- solution (pipette) was -6.3 ± 4.4, -7.5 ± 4.9, or - 45.8 ± 8.5 mV, respectively. Niflumic acid (100 μM) reversibly blocked the inward current, which was also blocked by 10 μM pyrilamine but not by 10 μM cimetidine. When histamine was continuously applied in the bath, spontaneous transient inward currents were generated. Removal of external Ca2+ or addition of 1 μM nicardipine or 2 mM caffeine reduced the amplitude of the histamine-induced inward current. These results suggest that histamine induces an inward current via H1 receptors at the resting membrane potential, possibly due to activation of Cl- currents. The Cl- inward current might be generated by elevation of intracellular Ca2+ via histamine receptors. The inward current may also contribute to control of the Ca2+ influx via a change in the membrane potential.
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||2 41-2|
|Publication status||Published - Feb 1997|
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine
- Physiology (medical)