Calcium currents in single isolated smooth muscle cells from the rabbit ear artery in normal‐calcium and high‐barium solutions.

Abstract

SUMMARY1. Ca2" inward current was studied using the whole-cell patch clamp technique in single smooth muscle cells enzymatically isolated from the rabbit ear artery.Currents were studied in salt solutions containing either normal (1-5 mM) Ca2`or high (110 mM) Ba2+. Outward currents were minimized by using a high-Na+ intracellular solution containing 10 mM-TEA.2. In normal-Ca2+ solution, the threshold at which inward current could be evoked was -60 mV at a holding potential of -80 mV and -48 mV at a holding potential of -60 mV. At both holding potentials, the current showed little inactivation over 500 ms near threshold, and inactivated substantially but incompletely with larger depolarizations. In high-Ba2+ solution where currents were 5-10 times larger, current threshold, maximal peak amplitude and apparent reversal potential were shifted in a positive direction along the voltage axis.3. Inward current in normal-Ca2+ solution was only fully available negative to -90 mV, was half-inactivated near -47 mV and was about 90% inactivated at -10 mV. A component of non-inactivating current was, however, present in both normal-Ca2' and high-Ba2+ solutions even after conditioning pulses of 5 s duration to + 30 mV. The inactivation-potential relationship was shifted in a positive direction in high-Ba2+ solution, and its position showed considerable variation between cells.4. The inward current from a holding potential of -70 mV was reduced in normalCa2+ solution by about 50 % by nifedipine (041 /tM) in some cells at all test potentials, although at more-negative test potentials peak current was unaffected in some cells even at 10 /iM. In some cells when the holding potential was -90 mV, the peak current amplitude was increased markedly by 10 /iM-nifedipine. In high-Ba2+ solution, from negative holding potentials (-70 to -80 mV), nifedipine augmented peak current at test potentials negative to -10 mV and shifted the current threshold in a negative direction; current at potentials positive of -10 mV was reduced. Both effects were concentration dependent. The stimulatory effect of nifedipine was abolished and its inhibitory effect was enhanced when less-negative holding potentials were employed. Bay K 8644 (0-1 or 1 /bM) approximately doubled current * Present address:

Effects of pinaverium on voltage‐activated calcium channel currents of single smooth muscle cells isolated from the longitudinal muscle of the rabbit jejunum

“…Inward current was 50% inactivated at -39mV (control, El) and at -40 mV in 1 jM pinaverium (-). Aaronson et al, 1988). Pinaverium (1 uM) had a small effect on Vh (-19 mV) if a IO s conditioning pulse was used (Figure 7b) although only a small change in Vh was seen (Vh = -9.6 mV) if a 2s conditioning pulse was used (Figure 7a).…”

Effects of captopril on membrane current and contraction in single ventricular myocytes from guinea‐pig

“…Jin et al, 1988). Aaronson et al (1988) have described a dihydropyridine-sensitive calcium current in vascular smooth muscle cells from rabbit ear artery. L-type Ca2+ current has been shown to be the predominant Ca2+ channel in coronary artery smooth muscle cells from guinea-pig (Ganitkevich & Isenberg, 1990).…”

Identification of the major membrane currents in freshly dispersed single smooth muscle cells of guinea‐pig ureter.

“…For example, in rabbit jejunum, rat vas deferens and guinea-pig bladder ica has an initial rapid decay (usually exponential with a time constant of 5-30 ms) which is followed by a slower exponential decay (time constant of 200-300 ms). In these cells ica is usually 90 % inactivated within 500 ms (Klockner & Isenberg, 1985b;Nakazawa et al 1987;Bolton, Aaronson & MacKenzie, 1988). In the rabbit ear artery ica has been divided into a exponentially decaying component superimposed on a sustained comnponent which does not inactivate even during a 5 s depolarization ).…”

“…In the rat vas deferens iCa is followed by a slowly activating iK which is not sensitive to raising the extracellular Ca2+ or to low concentrations of the Ca2+-entry blocker, nicardipine (Nakazawa et al 1987). In single vascular cells, depolarization generally triggers a large outward K+ current (Bean, Sturek, Puga & Hermsmeyer, 1986;Okabe, Kitamura & Kuriyama, 1987;Aaronson, Bolton, Lang & MacKenzie, 1988) although it may sometimes be preceded by a small transient ica (Toro & Stefani, 1987;Yatani, Seidel, Allen & Brown, 1987). A portion of this K+ current is also sensitive to Ca2+-entry blockade and exposure to TEA.…”