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At least 577 records · Page 32Linked to original sources
PubMed1990

Potassium channel blockers and the effects of cromakalim on the smooth muscle of the guinea-pig bladder.

1. The K+ channel blocking drugs tetraethylammonium Cl (TEA), procaine, 4-aminopyridine (4AP) and quinidine all produced concentration-dependent contractions of strips of smooth muscle from the guinea-pig urinary bladder. Apamin and glibenclamide caused little increase in the mechanical activity, and tolbutamide inhibited it. 2. TEA, procaine, 4AP, quinidine and apamin all increased the frequencies of spontaneous action potentials recorded with microelectrodes. TEA, quinidine and procaine all caused prolongation of the falling phase of the spike, and procaine and apamin completely abolished the after-hyperpolarization. 3. TEA and procaine increased K+ efflux from the tissue, an effect blocked by nifedipine. TEA and apamin increased, whereas quinidine, procaine and 4AP decreased K+ uptake. 4. Cromakalim caused a concentration-dependent hyperpolarization of the membrane, abolished spike activity, increased K+ fluxes and relaxed the smooth muscle. The relaxant effect of cromakalim was unaffected by apamin, and in its presence the effects of cromakalim on membrane potential and K+ fluxes were unchanged. Procaine abolished all the effects of cromakalim, and TEA at high concentrations reduced but did not abolish these effects. Quinidine reduced the effects of cromakalim on tension and membrane potential, but its actions were surmounted by higher concentrations of cromakalim. The effects of 4AP on tension and membrane properties were transitory, but it had some effects on the actions of cromakalim. Glibenclamide and tolbutamide reversed the relaxant effects of submaximal cromakalim concentrations, tolbutamide only transiently. 5. It is concluded that the channels opened by cromakalim are not those involved in generating the spike after-hyperpolarization. They have properties similar to the delayed rectifier K+ channels responsible for spike repolarization, and also are similar to the ATP-dependent K channels in vascular smooth muscle.

4-Aminopyridine↗
PubMed1987

Cellular calcium regulates outward currents in rabbit intestinal smooth muscle cell.

The nature of transient and oscillatory outward currents (ITO and IOO) in fragmented smooth muscle cells (smooth muscle ball, SMB) from the longitudinal muscle layer of the rabbit ileum, was studied using a single electrode voltage clamp technique. With a high K+ solution containing 0.3 mM ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid (EGTA) in the pipette and physiological salt solution (PSS) in the bath, the Ca inward current was followed by a large transient outward current (ITO) and spontaneous oscillations of the outward current (IOO) on the sustained outward current (ISO) were elicited by a depolarizing pulse, positive to -30 mV (holding potential of -60 mV). When the internal fluid of the SMB was replaced with Cs+-tetraethylammonium+ (TEA+) solution, or when the concentration of EGTA in the pipette was increased to 4 mM, using the intracellular perfusion technique, both ITO and IOO were abolished. In Mn2+ solution both currents were also inhibited. Bath application of TEA+, procaine or A23187 completely blocked both ITO and IOO. Caffeine (0.3-1 mM) enhanced the amplitude of ITO and generations of IOO, and concentrations of caffeine over 3 mM transiently enhanced, but finally suppressed both these currents. These results suggest that the generation of ITO is closely related to the Ca2+ influx, whereas the generation of IOO may be initiated by an increment in the intracellular concentration of Ca2+, possibly released from store sites.

Animals↗
PubMed1982

Calcium-dependent contractile activation of cerebral artery produced by quick stretch.

Quick stretch of helical strips of rabbit basilar artery at a rate of 4-50 cm/s to 140% of the initial muscle length evoked phasic contraction. The contraction was potentiated by cardiac glycosides, tetraethylammonium, and high K+, all of which augment transmembrane influx of Ca2+, and the enhanced response was suppressed by Ca2+-antagonists such as verapamil and nifedipine. The stretch-induced contraction in Ca2+-free medium was progressively reduced depending on the number of stretches during the observation period of 90 min. The response to quick stretch in Ca2+-free solution was enhanced by norepinephrine or histamine but was not affected by high K+ (40-100 mM), verapamil, or nifedipine. These results suggest that contraction of rabbit basilar artery produced by quick stretch depends not only on transmembrane supply of Ca2+ but also on release of Ca2% bound to the membrane or in internal depots. It also seems possible that, in addition to depolarization of the membrane, mechanical deformation itself triggers the release of Ca2+.

Amines↗
PubMed1977

Effects of ions and drugs on the negative afterpotential in the longitudinal muscle of pregnant rat myometrium.

Effect of Na, Ca anions and drugs (isoprenaline, TEA, procaine) on the negative afterpotential in the longitudinal muscle of pregnant rat myometrium were investigated using the double sucrose gap method. The negative afterpotential having a peak amplitude of about 15 mV decayed initially rapidly then slowly, the total duration being about 1 sec. Raising the external Ca concentration up to 10 mM or reducing Na to 54 mM increased the amplitude of the negative afterpotential. Replacement of Cl with Br enhanced the negative afterpotential and and replacement with benzene sulphonate or isethionate depressed it. The application of 10 mM TEA increased, while 10 mM procaine reduced the amplitude of both spike and negative afterpotential. 10(-10)-107(-8)g/ml isoprenaline depressed the negative afterpotential dosedependently, while leaving the spike potential nearly unaffected. It was concluded that the negative afterpotential was composed of a least two ionic mechanisms, one of Cl origin, the other of Ca origin.

Animals↗