Contraction In Guinea-pig Taenia Coli Research Articles

Effects of zinc ions on Ca2+ uptake during histamine-induced contraction in guinea-pig taenia coli.

The present study was undertaken to clarify the effects of zinc ions (Zn2+) on Ca2+ uptake during histamine-induced contraction in guinea-pig taenia coli. Zn2+ (0.3 mM) had smaller effect on the initial phasic response to 10(-5) M histamine accompanied with decreased Ca uptake at the high affinity sites, while it inhibited the tonic response by inhibiting Ca2+ uptake at the low affinity sites. After the first stimulation with histamine in the presence of Zn2+, the Ca2+ binding at high affinity sites was not significantly recovered in the presence of Zn2+. A second stimulation with histamine in the presence of Zn2+ did not elicit any phasic response. Furthermore, after beta-escin treatment of the fibres, which leaves receptor-coupled signal transduction including the Ca2+ storage sites intact, the contraction due to 10(-5) M histamine was not so affected by 0.3 mM Zn2+, but, after resuspension in a solution of pCa 5, 10(-5) M histamine of second application did not elicit the contraction in the presence of Zn2+. These results suggested that Zn2+ does not affect the histamine-induced Ca2+ release from the intracellular storage sites in taenia coli. However, when Zn2+ is present, Ca2+ is not supplied to the storage sites for the phasic response due to second stimulation with histamine. In addition, Zn2+ reduced the tonic response to histamine mainly by inhibiting Ca2+ influx through receptor-operated and/or voltage-dependent Ca2+ channels.

P-546 - Effect of Y-27362 on the spontaneous contraction of guinea-pig taenia coli

P-546 - Effect of Y-27362 on the spontaneous contraction of guinea-pig taenia coli

P–331 - Mechanism of leukotriene C4 induced contraction in guinea-pig taenia coli

P–331 - Mechanism of leukotriene C4 induced contraction in guinea-pig taenia coli

Contractile action of Mn2+ via Ca2+ channels activated by bay K 8644 in guinea-pig taenia coli.

Mn2+ has been shown to inhibit K+-induced contraction of smooth-muscle, to induce contraction of smooth-muscle in Ca2+-free, K+ medium and to activate the contractile proteins of skinned fibres of smooth muscle cells. Further work has suggested that Mn2+ penetrates the cytoplasm through voltage-dependent Ca2+ channels when the cell membranes of smooth muscles are depolarized with K+. We have investigated whether in Ca2+-free medium, Mn2+ enters the cytoplasm through Ca2+ channels and induces contraction of guinea-pig taenia coli in the presence of Bay K 8644, a dihydropyridine Ca2+-channel agonist which prolongs the open state of the voltage-dependent Ca2+ channels in smooth-muscle cells. In Ca2+-free medium the application of 5 mM Mn2+ in the presence of Bay K 8644 caused contraction of and concomitant increase in Mn2+ uptake in guinea-pig taenia coli smooth muscle. In the presence of Bay K 8644 nifedipine, a dihydropyridine Ca2+ channel antagonist, dose-dependently inhibited both manganese uptake and the contraction induced by Mn2+. These results suggest that Mn2+ enters the cytoplasm through dihydropyridine-sensitive, voltage-dependent Ca2+ channels activated by Bay K 8644 and then induces contraction in taenia coli.

Inhibitory action of PPADS on relaxant responses to adenine nucleotides or electrical field stimulation in guinea‐pig taenia coli and rat duodenum

1. The effect of pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS) on the relaxant response to adenine nucleotides was examined in the carbachol-contracted guinea-pig taenia coli and rat duodenum, two tissues possessing P2y-purinoceptors. In addition, in the taenia coli PPADS was investigated for its effect on relaxations evoked by adenosine, noradrenaline and electrical field stimulation. In order to assess the selectivity of PPADS between P2-purinoceptor blockade and ectonucleotidase activity, its influence on ATP degradation was studied in guinea-pig taenia coli. 2. The resulting rank order of potency for the adenine nucleotides in guinea-pig taenia coli was: 2-methylthio ATP >> ATP > alpha,beta-methylene ATP with the respective pD2-values 7.96 +/- 0.08 (n = 23), 6.27 +/- 0.12 (n = 21) and 5.88 +/- 0.04 (n = 24). 3. In guinea-pig taenia coli, PPADS (10-100 microM) caused a consistent dextral shift of the concentration-response curve (CRC) of 2-methylthio ATP and ATP resulting in a biphasic Schild plot. A substantial shift was only observed at 100 microM PPADS, the respective pA2-values at this particular concentration were 5.26 +/- 0.16 (n = 5) and 5.15 +/- 0.13 (n = 6). Lower concentrations of PPADS (3-30 microM) antagonized the relaxant effects to alpha,beta-methylene ATP in a surmountable manner. An extensive shift of the CRC was produced only by 30 microM PPADS (pA2 = 5.97 +/- 0.08, n = 6), and the Schild plot was again biphasic. 4. The relaxant responses to electrical field stimulation (80 V, 0.3 ms, 5 s, 0.5-16 Hz) in guinea-pigtaenia coli were concentration-dependently inhibited by PPADS (10-100 microM).5. In guinea-pig taenia coli, the potency of ATP in inducing relaxation appeared to be independent of its rate of degradation by ecto-nucleotidases, since the Km-value (366 microM) obtained in the enzyme assay was much higher than the functional EC50-value (0.45 microM) of ATP. PPADS (3-100 microM) was only weakly active in inhibiting ecto-nucleotidase activity leaving a residual activity of 81.8 +/- 5.1% at 100 microM.Enzyme inhibition by PPADS was concentration-independent and non-competitive.6. In rat duodenum, the rank order of potency was: 2-methylthio ATP >ATP> >alpha,beta-methylene ATP,the respective pD2-values being 6.98 +/- 0.04 (n = 76), 6.26 +/- 0.02 (n = 6) and 4.83 +/- 0.02 (n = 6). Among these agonists, 2-methylthio ATP displayed the lowest apparent efficacy.7. The CRC of 2-methylthio ATP in rat duodenum was shifted to the right by PPADS (10-100 microM) ina concentration-dependent manner, and Schild analysis gave a pA2-value of 5.09 +/- 0.06 (slope = 1.02,n=14).8 PPADS was without any effect on the carbachol-induced contraction in guinea-pig taenia coli or rat duodenum and on the relaxation to noradrenaline or adenosine in guinea-pig taenia coli.9 In conclusion, the antagonistic properties of PPADS at the taenia coli and rat duodenum P2y-purinoceptors were different from those recently described at the P2x-subtype: inhibition of P2y-purinoceptor-mediated responses was observed at higher concentrations (3-100 microM vs. 1-10 (30) microM).Furthermore, we conclude that in addition to the classical P2y-subtype, which is largely PPADS-resistant,the guinea-pig taenia coli may be endowed with a distinct relaxation-mediating P2-purinoceptor subtype which is sensitive to PPADS.

Protein tyrosine phosphorylation, cellular Ca2+, and Ca2+ sensitivity for contraction of smooth muscle.

Our studies are guided by the novel hypothesis that protein tyrosine phosphorylation is an important mechanism for regulating contraction of smooth muscle. Several lines of evidence are reviewed which suggest that enhanced tyrosine phosphorylation participates in mechanisms that regulate cytosolic Ca2+ and Ca2+ sensitivity for contraction. First, vanadate-induced contraction of guinea-pig taenia coli is functionally linked to enhanced protein tyrosine phosphorylation of at least three substrates, apparently resulting from vanadate-mediated inhibition of protein tyrosine phosphatase activity. Second, vanadate-induced contraction is dependent on extracellular Ca2+. Third, increases in cytosolic Ca2+ resulting from stimulation of alpha 1-adrenergic receptors in cultured canine vascular smooth muscle cells are associated with enhanced tyrosine phosphorylation and are inhibited by genistein, a potent inhibitor of tyrosine kinase activity. Fourth, genistein markedly and reversibly suppresses Ca2+ sensitivity for contraction in ileal longitudinal smooth muscle permeabilized with staphylococcal alpha-toxin. Moreover, the same or similar substrates (e.g., 42-45, 70, 80-85, 95, 100, 110, 116, and 205 kDa) are tyrosine phosphorylated in response to Ca2+ or stimulation of muscarinic or alpha 1-adrenergic receptors. Collectively, these data strongly suggest that tyrosine phosphorylation is an important mechanism for regulation of smooth muscle contraction.

Calcium antagonism by cobalt ions on contraction of guinea-pig taenia coli.

In guinea-pig taenia coli, cobalt ions (Co2+) inhibited the tonic response to a highly concentrated K+ solution (high-K+, 40 mM) more strongly than the phasic response. Co2+ displaced Ca2+ concentration-response curves to the right, inhibited the increase in tissue calcium content caused by high-K+, and inhibited Ca2+ binding at low affinity sites more than at high affinity sites. After treatment with Co2+, the tonic tension caused by high-K+ was not restored by a wash with normal medium, but it was restored by a wash with EDTA. The cobalt remaining in muscles was almost completely eliminated after a 20-30 min wash with EDTA. The results suggest that Co2+ binds chiefly to the surface membrane of taenia coli. Co2+ probably reduced the tension in response to high-K+ mainly by inhibiting Ca2+ influx rather than by affecting Ca2+ release.

Two phases of the prostaglandin F2?-induced contraction in guinea-pig taenia coli involve different Ca2+ channels

Properties of the contraction produced by PGF2 alpha in the guinea-pig taenia coli were compared to those produced by ACh. Prostaglandin (PG) F2 alpha (3 x 10(-7) M) and acetylcholine (ACh, 10(-5)M) induced an initial transient contraction (phasic contraction) and a subsequent late contraction (tonic contraction). Both phasic and tonic contractions produced by PGF2 alpha or ACh were abolished in Ca2+ -free Krebs solution containing 0.5 mM EGTA. The tonic contractions caused by PGF2 alpha and ACh were markedly suppressed by alpha-[3-[[2-(3,4-dimethoxy-phenyl)-ethyl]-methylamino]-propyl]- 3,4,5-trimethoxy-alpha-(1-methylethyl)benzeneacetonitrile hydrochloride (D600, greater than 10(-7)M) as well as nifedipine (5 x 10(-9)M), a Ca2+-antagonist. However, the phasic contraction produced by PGF2 alpha, but not by ACh, was greatly inhibited by Mn2+ (greater than 10(-4)M). Furthermore, the phasic contraction caused by PGF2 alpha was abolished in 18 mM K+ Krebs solution with D600 (2 x 10(-7)M), whereas that induced by ACh and the tonic contractions produced by PGF2 alpha as well as by ACh were unaffected in this high K+ solution without D600. Membrane potentials of the tissue in normal (K+, 5.9 mM) and 18 mM K+ Krebs solution containing D600 were about -55 mV and -43 mV, respectively. In a fluorescence study which used Fura-2 an intracellular free Ca2+ indicator in the presence of D600, PGF2 alpha and ACh increased fluorescence intensity in the tissue, which coupled with the magnitude of contractions.(ABSTRACT TRUNCATED AT 250 WORDS)

Inhibitory effect of beauvericin on a high K+-induced tonic contraction in guinea-pig taenia coli.

An inhibitory effect of beauvericin, a cyclodepsipeptide, on a high K+-induced contraction in guinea-pig taenia coli was compared with those of verapamil, an organic Ca2+ antagonist, and monensin, an inhibitor of mitochondrial respiration. Beauvericin (10(-5) M), verapamil (5 x 10(-7) M) or monensin (10(-6) M) markedly inhibited the tonic contraction, while these drugs showed less effect on the phasic contraction. Beauvericin at a lower concentration (10(-6) M) competitively inhibited the Ca2+-induced contraction in depolarized muscle, whereas higher concentrations (3 x 10(-6) or 10(-5) M) non-competitively inhibited this contraction. Verapamil (10(-8)-5 x 10(-7) M) competitively inhibited and monensin at a low concentration (10(-7) M) non-competitively inhibited this contraction. A contraction induced by 0.5 mM Ca2+ was inhibited by beauvericin with an IC50 (concentration needed for 50% inhibition) of 2.8 x 10(-7) M, verapamil with an IC50 of 2.9 x 10(-8) M, and nifedipine with an IC50 of 1.8 x 10(-9) M. 10(-6) M CGP 28392, a Ca2+ channel facilitator, increased the IC50 of beauvericin, verapamil or nifedipine. Although the inhibitory effect of monensin (10(-7)-10(-6) M) on the high K+-induced contraction was reduced under hypoxia, the effects of beauvericin (10(-7)-10(-5) M) and verapamil (10(-8)-10(-7) M) were not modified. Beauvericin (10(-5) M) changed neither the intracellular Na+ and K+ contents of the depolarized muscle nor the Ca2+-induced contraction in the chemically skinned taenia coli.(ABSTRACT TRUNCATED AT 250 WORDS)

Inhibitory Effect of Beauvericin on a High K+-lnduced Tonic Contraction in Guinea-Pig Taenia Coli

An inhibitory effect of beauvericin, a cyclodepsipeptide, on a high K+-induced contraction in guinea-pig taenia coli was compared with those of verapamil, an organic Ca2+ antagonist, and monensin, an inhibitor of mitochondrial respiration. Beauvericin (10-5 M), verapamil (5×10-7 M) or monensin (10-6 M) markedly inhibited the tonic contraction, while these drugs showed less effect on the phasic contraction. Beauvericin at a lower concentration (10-6 M) competitively inhibited the Ca2+-induced contraction in depolarized muscle, whereas higher concentrations (3×10-6 or 10-5 M) non-competitively inhibited this contraction. Verapamil (10-8-5×10-7 M) competitively inhibited and monensin at a low concentration (10-7 M) non-competitively inhibited this contraction. A contraction induced by 0.5 mM Ca2+ was inhibited by beauvericin with an IC50 (concentration needed for 50% inhibition) of 2.8×10-7 M, verapamil with an IC50 of 2.9×10-8 M, and nifedipine with an IC50 of 1.8×10-9 M. 10-6 M CGP 28392, a Ca2+ channel facilitator, increased the IC50 of beauvericin, verapamil or nifedipine. Although the inhibitory effect of monensin (10-7-10-6 M) on the high K+-induced contraction was reduced under hypoxia, the effects of beauvericin (10-7-10-5M) and verapamil (10-8-10-7 M) were not modified. Beauvericin (10-5 M) changed neither the intracellular Na+ and K+ contents of the depolarized muscle nor the Ca2+-induced contraction in the chemically skinned taenia coli. These results suggest that the inhibitory action of beauvericin (10-5 M) on the high K+-induced tonic contraction is due to the non-competitive inhibition of Ca2+ entry through the voltage-dependent Ca2+ channel of the intestinal smooth muscle cell.

On the inhibitory mechanism of bassianolide, a cyclodepsipeptide, in acetylcholine-induced contraction in guinea-pig taenia coli.

The effect of bassianolide (BASS), a cyclodepsipeptide, was investigated on mechanical response, membrane potential, intracellular Na and K contents and 45Ca uptake in response to acetylcholine (ACh) in guinea-pig taenia coli. BASS (10(-5) M) as well as verapamil (5 X 10(-7) M) and papaverine (3 X 10(-5) M) selectively inhibited the tonic component of the contraction induced by ACh (10(-5) M), but scarcely affected the phasic one. In contrast, atropine (3 X 10(-8) M) inhibited both components of contraction. BASS did not modify the change in membrane potential by ACh. BASS, ACh and the combination of both did not influence the intracellular Na and K contents and the 45Ca uptake. These data show that BASS seems unlikely to have the property of an ionophore. BASS slightly inhibited both the tonic and phasic components of contraction induced by 60 mM K in a non-selective manner, though verapamil and papaverine inhibited the tonic component more potently than the phasic one. Verapamil decreased the increased 45Ca uptake in the muscle soaked in 60 mM K medium, but BASS did not. Since BASS selectively inhibits the tonic component of the ACh-induced contraction, the inhibitory mechanism of BASS seems to be different from that of verapamil, papaverine or atropine; and the mechanism may be beyond the interactions with a binding activity of ACh to the muscarinic receptor, membrane potential and the contractile machinery of the intestinal smooth muscle.

Effects of calmodulin antagonists on tension and cellular calcium content in depolarized vascular and intestinal smooth muscles.

1 Several putative calmodulin antagonists have been examined for their inhibitory action on muscle tension and cellular Ca content in the K-depolarized vascular and intestinal smooth muscles. 2 The 65.4 mM K-induced sustained contraction in the media-intimal layer of rabbit aorta and the 45.4 mM K-induced sustained contraction in guinea-pig taenia coli were inhibited by the calmodulin antagonists, prenylamine, chlorpromazine, N2-dansyl-L-arginine-4-t-butylpiperadine amide (No. 233), and N-(6-aminohexyl)-5-chloro-1-naphthalenesulphonamide (W-7), and also by the organic Ca antagonists, verapamil and diltiazem. 3 The cellular Ca content in rabbit aorta and guinea-pig taenia coli as measured by a modified lanthanum technique increased in the high-K solutions. The increments were inhibited by these antagonists at concentrations similar to those required to inhibit the K-induced contractions. However, W-7 did not change (in aorta) or only slightly decreased (in taenia coli) the K-induced increase in the cellular Ca content. 4 A high concentration (2 X 10(-4)M) of W-7 increased the resting cellular Ca content without increasing the muscle tension in aorta. The increment was inhibited by verapamil, sodium nitroprusside or hypoxia (N2 aeration). 5 It is suggested that the inhibitory effects of prenylamine, chlorpromazine and No. 233 may be attributed mainly to the Ca antagonistic effect whereas W-7 may inhibit the process beyond the transmembrane Ca influx.

The inhibitory effect of monensin on high K-induced contraction in guinea-pig taenia coli.

This study deals with the effects of monensin, a Na ionophore, on contraction, cellular Na content, oxygen consumption and tissue ATP content of smooth muscle of the guinea-pig taenia coli depolarized by high K (62.7 mM) solution. The application of monensin (10(-8) -10(-6) M) had little effect on the phasic component of the K contraction while it decreased the tonic component. The inhibitory effect of monensin, unlike that of verapamil, was not antagonized by raising the concentration of external Ca. Under hypoxic conditions, the inhibitory action of monensin (10(-7) M) was greatly reduced. The removal of Na (choline or sucrose substitution) from the high K solution did not attenuate the inhibitory effect of hypoxia or monensin. Monensin (10(-7) M) produced only a small increase in cellular Na in the depolarized muscle. The K-induced increase in the rate of oxygen consumption was suppressed by monensin (10(-6) M). In high K solution, but not in normal solution, monensin (10(-6) M) decreased the tissue ATP content. These results suggest that the relaxing action of monensin is mainly due to the inhibition of aerobic energy metabolism of the smooth muscle of guinea-pig taenia coli.

Effects of hydralazine and verapamil on phosphorylase activity and guanosine cyclic 3',5'-monophosphate levels in guinea-pig taenia coli.

1 The roles of guanosine cyclic 3',5'-monophosphate (cyclic GMP) and calcium in the relaxation produced by hydralazine and verapamil in potassium-depolarized guinea-pig taenia coli have been investigated.2 Depolarization of isolated strips of guinea-pig taenia coli by 124 mM KCl caused sustained contractures and increases in tissue levels of cyclic GMP.3 The KCl-induced increases in cyclic GMP levels appeared to be calcium dependent. No increases in cyclic GMP levels were seen in strips of taenia coli depolarized in the absence of calcium. Readdition of calcium to the depolarizing solution contracted the muscles and increased cyclic GMP levels. When calcium was removed from the depolarizing solution during the sustained, tonic phase of a KCl-induced contracture, both tension and cyclic GMP levels returned to control values.4 Administration of 50 muM verapamil to KCl-contracted muscles completely relaxed the muscles and caused cyclic GMP levels to return to control values within 14 min. Hydralazine, 2 mM, on the other hand, relaxed the depolarized muscles without lowering cyclic GMP levels. No significant changes in cyclic AMP levels were seen in any of these experiments.5 Similar results were obtained in an analogous series of experiments in which glycogen phosphorylase activity was measured instead of cyclic GMP levels. Activation of phosphorylase during contractions of guinea-pig taenia coli had previously been reported to be a calcium-dependent phenomenon.6 It was concluded that increases in tissue levels of cyclic GMP (or of cyclic AMP) were not responsible for the relaxant effects of hydralazine or verapamil in these experiments. It was also suggested, based on our results, that verapamil exerted its relaxant effects in the depolarized taenia coli by lowering cytoplasmic calcium levels, whereas hydralazine relaxed the depolarized muscles without lowering intracellular calcium activity.

The inhibitory effect of lithium of high-K induced contraction in guinea-pig taenia coli.

1. This study deals with the effects of lithium (Li) on the membrane potential, tension development, intracellular Na, K and Li contents and 45Ca uptake of smooth muscle of the guinea-pig taenia coli depolarized by high-K (62.7 mM) solution. 2. Replacement of Na with Li in high-K solution resulted in a concentration-dependent inhibition of muscle contraction without affecting membrane depolarization. The effect of Li-substitution was also dependent on the duration of exposure to Li and was antagonized by raising the concentration of external Ca ([Ca]0). Replacement of Na with tris (hydroxymethyl) aminomethane (Tris), sucrose or choline did not show such an inhibitory effect. 3. To estimate the intracellular Na content by removing extracellular bound Na, muscle strips were washed with cold Li solution and the amount of Na remaining in the tissue was measured. During washout with the cold Li-solution, a part of the tissue Na was rapidly lost followed by a rapid Li uptake while the remaining Na was lost very slowly as a single exponential process. A similar change in tissue Li level was observed in Li-loaded tissue during washout with cold Na-solution. The residual Na and Li after a 1 h washout with the cold solutions were regarded as intracellular Na and Li, respectively. 4. Replacement of a part of the extracellular Na in high-K solution with either Li or sucrose led to a slight decrease in intracellular Na. In the case of Li substitution, Li gradually accumulated in the muscle cells. The increase in intracellular Li was dependent on the concentration of external Li. 5. The relaxation produced by Li was correlated with the intracellular Li content of the tissues. Both the Li-induced relaxation and the increased intracellular Li were fully reversible with similar time courses following removal of extracellular Li. 6. 45Ca uptake of the muscle measured by a modified “La-method” increased in high-K solution. This increase was inhibited by a pretreatment with Li. 7. It is suggested that the action of Li is closely related to an accumulation of intracellular Li, which may produce muscle relaxation mainly by inhibiting the depolarization-induced Ca influx.

The effects of amrinone on contractility, Ca 2+ uptake and cAMP in smooth muscle

Amrinone, a known positive inotropic agent in the heart, was found to cause a dose-dependent (10–100 μg/ml) inhibition of norepinephrine (NE) or high-K +-induced contractions of rabbit aorta. Amrinone also inhibited carbachol or high-K +-induced contractions of guinea-pig taenia coli. Neither total tissue 45Ca uptake nor the rate of 45Ca uptake induced by 80 mM K + in rabbit aorta was altered by pretreatment with amrinone. On the other hand, a similar pretreatment with amrinone inhibited NE (10 −6 or 10 −5 M) induced tissue 45Ca uptake. Amrinone (100 μg/ml) caused about a 70% increase in cAMP concentration over resting levels. It is concluded that amrinone causes a nonspecific inhibition of smooth muscle contractility by acting probably at multiple sites to decrease the availability of Ca 2+ required for activation. One or more of these mechanisms may involve cAMP.

Stimulating effects of alanine and glycine on guinea-pig taenia coli (author's transl)

Effects of alanine and glycine on the mechanical and electrical activities of guinea-pig taenia coli were investigated. Alanine (0.1--10 mM) and glycine (0.5--10 mM) produced a dose dependent contraction of guinea-pig taenia coli. The stimulating effects of alanine and glycine were not inhibited in the presence of atropine (5 muM), tetrodotoxin (0.1 micrograms/ml), diphenhydramine (4 muM), methysergide (3 muM), strychnine (10 muM), and were not influenced by treatment with indomethacin (3 muM). However, these effects were inhibited in the presence of a Ca antagonist, verapamil (10 muM). When the electrical activities of the taenia coli were recorded by the single sucrose-gap method, alanine and glycine (5--10 mM) produced a reduction of membrane potential and increased spike heights and frequencies of action potential. In LiCl or Choline-Cl and in Na-isethionate solutions, the stimulating effect of alanine was not abolished, but was completely inhibited in KCl-depolarized preparation. From these results, it is considered that both alanine and glycine may directly produce contraction by a depolarization of the cell membrane of guinea-pig taenia coli.

188 - Effects of diethylstilbestrol and D-600 on Ca-free contraction in guinea-pig taenia coli

188 - Effects of diethylstilbestrol and D-600 on Ca-free contraction in guinea-pig taenia coli

Sodium in smooth muscle relaxation.

The contraction of guinea-pig taenia coli due to high K+ could not be reversed by washing when Na+ was absent from the medium. Reintroduction of Na+ (7 mM or more) caused relaxation. Similar results were obtained with rat uterus. The effect of sodium replacement was not due to change in ionic strength because equal or higher osmoles of choline, Ca++, K+, Mn++, or Mg++ had little or no effect. Persistence of contraction in the Na+-free medium was not due to a "catch state" of the contractile apparatus. Impairment of Ca+ removal from the cytoplasm rather than persistent increase in Ca+ influx seemed to sustain the mechanical response. This was because D600 (a calcium influx blocker) failed to completely relax K+-induced contraction in the absence of Na+ and also because the ability of EGTA to produce relaxation was reduced in the absence of Na+. Measurement of tissue calcium content using the lanthanum method revealed coincident decrease in tissue calcium and tension to control level during Na+-mediated relaxation. The results suggest a role for transmembrane Na+-Ca++ exchange in causing the Na+-mediated relaxation of taenia undergoing Na+-free contracture.

18) - Isometric and isotonic contractions of guinea-pig taenia coli: effect of varying external Ca concentrations, anoxia, atropine and papaverine

18) - Isometric and isotonic contractions of guinea-pig taenia coli: effect of varying external Ca concentrations, anoxia, atropine and papaverine