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At least 145 records · Page 8Linked to original sources
PubMed1986

Mechanical and electrical aspects of the relaxant action of aminophylline in guinea-pig isolated trachealis.

Aminophylline (1-1000 mumol l-1) suppressed the spontaneous tone of guinea-pig isolated trachealis in a concentration-dependent manner. In Krebs solution containing acetylcholine (1 mmol l-1), histamine (200 mumol l-1) or K+ (120 mmol l-1) isolated trachealis muscle developed near-maximal tension. The log concentration-effect curve for aminophylline was shifted 20 fold, 3 fold and 4 fold to the right, respectively, in the presence of these spasmogens. Three K+-channel inhibitors were tested: tetraethylammonium (TEA, 8 mmol l-1) did not modify the action of aminophylline, procaine (5 mmol l-1) shifted the log concentration-effect curve for aminophylline 2 fold to the left and 4-aminopyridine (5 mmol l-1) shifted the curve 2.5 fold to the right. Intracellular electrophysiological recording showed that aminophylline 10 mumol l-1 could cause relaxation in the absence of electrical changes. Higher concentrations of aminophylline (100-1000 mumol l-1) suppressed spontaneous slow waves and hyperpolarized the trachealis cells. In the presence of procaine (5 mmol l-1) or TEA (8 mmol l-1), the hyperpolarization induced by aminophylline (1000 mumol l-1) was significantly reduced but its relaxant effect was unchanged. In trachealis skinned of its plasma membranes, tension development induced by Ca2+ (20 mumol l-1) was unaffected either by aminophylline (1000 mumol l-1) or by isoprenaline (1 mumol l-1). In studies of the efflux of 86Rb+ from muscle-rich strips of trachea, aminophylline (100-1000 mumol l-1) was without effect whereas nicorandil (100 and 1000 mumol l-1) increased the efflux rate constant. It is concluded that aminophylline does not directly reduce the sensitivity of the contractile proteins to cytosolic Ca2+. In low concentration (1-10 mumol l-1) its relaxant action is not accompanied by membrane potential change but towards the upper end of its effective concentration range, aminophylline evokes hyperpolarization. This hyperpolarization may involve the opening of K+-channels which are inhibited by procaine and (to a lesser extent) by TEA. These K+-channels may be impermeable to 86Rb+.

Acetylcholine↗
PubMed1988

Spasmogen action in guinea-pig isolated trachealis: involvement of membrane K+-channels and the consequences of K+-channel blockade.

1. Acetylcholine (ACh), histamine, prostaglandin E2 and potassium chloride (KCl) each evoked concentration-dependent spasm of guinea-pig isolated trachealis treated with indomethacin (2.8 microM). 2. Neither tetraethylammonium (TEA; 0.1-10 mM) nor procaine (0.1-10 mM) potentiated these spasmogens. Indeed, procaine (10 mM) depressed the log concentration-effect curves of all the spasmogens while TEA (1-10 mM) caused some depression of the log concentration-effect curve of prostaglandin E2. 3. Intracellular electrophysiological recording was performed in trachealis bathed by normal Krebs solution or by Krebs solution containing 2.8 microM indomethacin. In either medium the majority of trachealis cells exhibited spontaneous electrical slow waves while some cells were electrically quiescent. In either medium the spasmogenic effects of ACh (1 mM) and histamine (0.2 mM) were accompanied by depolarization and abolition of slow wave discharge. In many cases the record of membrane potential subsequently exhibited noise which incorporated fast, hyperpolarizing transients. 4. In the absence and presence of indomethacin, TEA (10 mM) and procaine (5 mM) markedly reduced the membrane noise and hyperpolarizing transients evoked by ACh or histamine without augmenting the evoked tension. 5. It is concluded that slow wave discharge does not depend on prostaglandin synthesis. The membrane noise and hyperpolarizing transients evoked by ACh and histamine represent the opening of membrane K+-channels. While such K+-channel opening may offset spasmogen-induced depolarization it does not moderate the evoked tension.

Animals↗
PubMed1981

Excitation--contraction coupling in smooth muscle cells of the guinea-pig mesenteric artery.

1. The excitation-contraction coupling mechanism in the smooth muscle of the guinea-pig mesenteric artery was studied using intact and chemically skinned muscle cells.2. The mean membrane potential of the intact smooth muscle was -65.8 +/- 2.4 mV. It was electrically quiescent. Caffeine (5 mm), procaine (> 1 mm) and TEA (> 1 mm) depolarized the membrane, increased the membrane resistance and in their presence, outward current pulses evoked action potentials with overshoot. These potential changes were still observed in Na-deficient solution but were abolished in the presence of 3 mm-MnCl(2).3. Caffeine (5 mm) and TEA (1 mm) produced contractions in the intact muscle which were suppressed by procaine (5-10 mm). Caffeine (5 mm) continued to produce contraction even after prolonged exposure to Ca-free solution (containing 2 mm-EGTA) and this contraction was suppressed by procaine (5 mm). On the other hand, the K-induced contraction was rapidly abolished in 0-Ca.4. Electrical stimulation (1 sec) in the presence of TTX (10(-7)m) evoked a contraction. Caffeine (5 mm) and TEA (5 mm) enhanced but procaine (5 mm) suppressed the contraction.5. Chemically skinned smooth muscle cells were prepared by adding saponin, 50 mug/ml., to the relaxing solution. The minimum concentration of free Ca required to evoke contraction in skinned muscle cells was 1-2 x 10(-7)m and the maximum contraction was produced at 10(-5)m. When Ca was replaced with Sr, the above relationship also shifted to the right (ED(50) for Ca is 4.4 x 10(-7)m and that for Sr is 1.5 x 10(-5)m). Treatment with high concentrations of caffeine and procaine had no effect on the pCa-tension relationship.6. Caffeine induced contraction in skinned muscle cells preloaded with Ca, and this contraction was markedly suppressed by procaine (5-10 mm).7. In skinned muscles, depolarization of the internal membrane by replacement of K with choline (116 mm) in the relaxing solution produced contraction, but the amplitude was much smaller than the caffeine-induced contraction.8. The relationship between the amplitude of caffeine-induced contraction and the duration of preincubation in various Ca concentrations was observed in skinned muscles. The minimum concentration of Ca required to produce a subsequent caffeine-induced contraction was itself below threshold for contraction. The results also indicate that the Ca-induced Ca release mechanism appears to modify the amount of Ca stored by preincubation in over 3 x 10(-7)m free Ca.9. When the amount of Ca stored in intact cells was estimated from the caffeine-induced contraction evoked in Ca-free solution following preincubation with Ca, Ca applied simultaneously with procaine increased and Ca with caffeine reduced the Ca stored in the cell. After preincubation in 2.5 mm-[Ca](o) with 1 mm-procaine for 5 min, the amplitude of the subsequently generated caffeine-induced contraction (5 mm) in Ca-free solution (2 min) was much the same as that observed in 118 mm-[K](o).10. The results support the view that the excitation-contraction coupling mechanism in the mesenteric artery may be as follows; the Ca inward current generated at the myoplasmic membrane may not directly provide the free Ca required to activate the Ca-receptor of the contractile protein, but the Ca carrying the inward current may first be sequestered inside the cell and activate a Ca release mechanism which in turn leads to contraction.

Animals↗