SUMMARY1. To investigate the mechanism of generation of contractions in tissues from the guinea-pig stomach, the effects of caffeine, procaine, acetylcholine (ACh), diltiazem or MnCl2 on the contraction evoked from small bundles of intact or skinned muscles (50 ,um in width and 250-300 ,um in length) were observed.2. All these agents except for ACh blocked the spontaneously generated contraction. Diltiazem (1 x 10-4 M) had no effect and MnCl2 (3 mM) slightly reduced and caffeine enhanced the tonic contraction evoked in Na-free solution, whereas procaine relaxed the tissue. On the other hand, in the isotonic [K]0 solution, diltiazem, MnCl2 and procaine relaxed the tissue, while caffeine enhanced the tonic contraction.3. Under pre-treatment with Ca-free solution (2 mM-EGTA-containing solution) after depletion of the stored Ca, application of 2-5 mM-Ca and subsequently applied 5 mM-caffeine produced contractions (Ca-and caffeine-induced contractions, respectively). In polarized (5-9 mM-K.) and depolarized (128 mM-KO) muscles, the various agents simultaneously applied with 2-5 mM-Ca modified the amplitude of the Ca-induced and the resulting caffeine-induced contractions. Thus, at least three different Ca influxes required to evoke the Ca-or caffeine-induced contraction were identified; diltiazem-sensitive Ca influx, diltiazem-insensitive but Mn-sensitive Ca influx and Mn-insensitive Ca influx.4. The Ca-and caffeine-induced contractions in Ca-free and 15-5 mM-Na-containing solutions were gradually reduced in amplitude, in proportion to the time of exposure. However, amplitude of the caffeine-induced contractions was inhibited to a greater extent and the duration of the contracts was less prolonged than the case of the Ca-induced contraction.5. In saponin-treated skinned muscles, the minimum concentration of Ca required to produce the contraction was 1 x 10-7 M, and the maximum contraction was evoked by application of 1 x 10-5 M-Ca. The effects ofNa-free solution on the Ca accumulation and release to and from the storage site were also observed in these skinned muscles.
1 Effects of acetylcholine (ACh) and noradrenaline (NA) on mechanical properties of smooth muscle cells of the guinea-pig portal vein were investigated using intact and skinned muscle preparations. In some preparations, the electrical activity was also recorded. In addition to ACh and NA, the effects of caffeine, procaine, excess concentrations of [K]0 and MnCl2 were investigated. 2 NA enhanced the mechanical response due to increase in the spike generation, receptor activated depolarization and release of Ca stored in the cell. 3 ACh also enhanced the mechanical response, but this agent had little effect on the Ca release from the storage sites. 4 Caffeine and procaine (10 mM) depolarized the membrane and enhanced the electrical activity. Caffeine enhanced the mechanical activity due to an increase in the membrane activity and the release of Ca stored in the cell, while procaine inhibited the contraction. Procaine inhibited and caffeine accelerated the Ca-induced Ca-release mechanism in the cell. NA released the Ca from the storage sites to a greater extent than did caffeine or ACh. 5MnCl2 inhibited the spontaneous membrane activity and contraction; however, low concentrations of MnCI2 increased the caffeine-or NA-induced contraction in Ca-free solution. 6 When the Ca-tension relationship was observed in saponin-treated skinned muscles, the minimum concentration of Ca required to produce the contraction was 10-7 M, as observed in other vascular tissues. Caffeine released the stored Ca, NA and ACh had no effect on the Ca release and procaine inhibited the caffeine-induced Ca release in skinned muscles. 7 It was concluded that the membrane properties of smooth muscle cells in the portal vein are much the same as observed in other spontaneously active visceral muscles. Differences observed in the actions of NA and ACh on mechanical properties seems to be mainly due to different receptoroperated Ca release mechanisms.
The properties of the tonic contraction evoked from smooth muscle cells of the guinea pig basilar artery by Na-free and isotonic [K], (143.6 mM K) solutions were investigated. In the Na-free solution (substituted by cyoline, Tris or sucrose), a small phasic contraction was followed by a large tonic one with 3-4 min latency. Diltiazem (1 >< 10*'*M) and MnCl2 (3 mM) had little elfect, while procaine (5 mM) completely relaxed the tissue. The tonic contraction evoked by the isotonic [K], solution was relaxed by diltiazem, MnCl, or procaine, and that evoked by the Nafree solution was relaxed at a very slow velocity by the addition of 1 mM [Na], or the removal of Ca. Caffeine (5 mM) produced a small or large phasic contraction superimposed on the tonic contraction evoked in the Na-free or isotonic [K], solution. The caffeine-induced contraction was followed by complete relaxation of the tissue in isotonic [K], solution, but not in Na-free solution. In saponin treated skinned muscles, the minimum concentration of Ca required to produce the contraction was 1 >< 10""M, and the maximum amplitude of contraction was evoked by application of 3 ><10""M Ca. This pCa-tension relationship was not affected by the presence or absence of Na in the relaxing solution. Furthermore, 10 mM procaine or caffeine only slightly inhibited the above relationship. In skinned muscles, accumulation of Ca into the storage site was slightly inhibited in the Na-free solution (0.85 times the control), as estimated from the amplitude of the resulting caffeine-induced contraction. However, Na-free solution had no effect on the leakage of Ca from the storage site. The present results indicate that the tonic contraction evoked in the Na-free solution is mainly due to inhibition of the Ca efflux at the myoplasmic membrane, while that evoked in the isotonic [K], solution is due to acceleration of the Ca influx.
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