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At least 865 records · Page 48Linked to original sources
PubMed1993

Inositol 1,4,5-trisphosphate releases Ca2+ from vacuolar membrane vesicles of Saccharomyces cerevisiae.

Inositol 1,4,5-trisphosphate (IP3) induces a release of Ca2+ from vacuolar membrane vesicles of Saccharomyces cerevisiae. The amount released is dependent on IP3 concentration (concentration for half maximal effect, Km, apparent = 0.4 microM). Myo-inositol, and inositol 1,4-bisphosphate up to 50 microM have no effect on Ca2+ levels in the vesicles. The IP3-induced Ca2+ release is blocked by dantrolene and 8-(N,N-diethylamino)-octyl 3,4,5-trimethoxybenzoate-HCl (TMB-8), which are known to block Ca2+ release from Ca2+ stores in animal cells. IP3-induced release of Ca2+ also occurs when Ca2+ is accumulated by means of an artificial pH gradient, indicating that the effect of IP3 is not due to an effect on the vacuolar H(+)-ATPase. The IP3-induced Ca2+ release is not accompanied by a change in the pH gradient, which indicates that it is not due to a reversal of the Ca2+/nH+ antiport or to a decrease in delta pH by IP3. The present results suggest that IP3 may act as a second messenger in the mobilization of Ca2+ in yeast cells. As in plant cells, the vacuolar membrane of yeast seems to contain a Ca2+ channel, which can be opened by IP3. In this respect the vacuole could function as an IP3-regulated intracellular Ca2+ store, equivalent to the endoplasmic- and sarcoplasmic reticulum in animal cells, and play a role in Ca(2+)-dependent signal transduction in yeast cells.

Adenosine Triphosphate↗
PubMed1991

Role of calcium in the control of steroidogenesis in preovulatory ovarian follicles of the goldfish.

The possible involvement of calcium in the regulation of steroidogenesis in the goldfish was investigated using preovulatory ovarian follicles incubated in vitro. Incubation of follicles in media deficient in calcium impaired testosterone production in response to human chorionic gonadotropin (hCG) in both the presence and the absence of the phosphodiesterase inhibitor IBMX. Similarly, addition of calcium channel antagonists (verapamil, nifedipine, nicardipine, and CoCl2) caused a dose-dependent inhibition of hCG-stimulated testosterone production. TMB-8, an inhibitor of intracellular calcium mobilization, also suppressed hCG-stimulated testosterone production. Basal testosterone production was not affected by incubation in calcium-deficient media or with drugs which reduce intracellular calcium availability. In other studies, nifedipine blocked forskolin and dibutyryl cyclic AMP-stimulated testosterone production suggesting that one of the major sites of calcium action is distal to cyclic AMP generation. Two inhibitors of calmodulin, W5 and W7, significantly inhibited hCG-stimulated testosterone production. These findings suggest that calcium derived from intracellular and extracellular pools participate in the expression of gonadotropin effects on steroid production in goldfish ovarian follicles and that these effects are mediated intracellularly by interaction with calmodulin.

Animals↗
PubMed1995

Lysophosphatidylcholine causes Ca2+ influx, enhanced DNA synthesis and cytotoxicity in cultured vascular smooth muscle cells.

The effects of lysophosphatidylcholine (LPC), a vasoactive phospholipid, on intracellular free calcium concentration ([Ca2+]i), DNA synthesis and cytotoxicity of vascular smooth muscle cells (VSMC) were studied. LPC from 10(-7) to 10(-5) mol/l dose-dependently induced a sustained increase in [Ca2+]i. In contrast to the response of [Ca2+]i induced by angiotensin II, that induced by LPC was totally abolished when extracellular Ca2+ was removed, was not affected by pretreatment of the cells with islet-activating protein, and was not desensitized by repeated addition. 8-(N,N-Diethylamino)octyl 3,4,5-trimethoxybenzoic acid (TMB-8), an inhibitor of Ca2+ release from intracellular Ca2+ stores, 1-(5-isoquinolinesulfonyl)-2-methylpiperadine dihydrochloride (H-7), an inhibitor of protein kinase C, KT5823, an inhibitor of protein kinase G, and Ca2+ channel blockers failed to suppress the LPC-induced increase in [Ca2+]i. LPC at 10(-5) mol/l caused significant stimulation of [3H]thymidine incorporation into VSMC, and at concentrations of 10(-5) mol/l and higher dose-dependently stimulated release of lactate dehydrogenase in cell culture supernatants. Moreover, digitonin mimicked the effects of LPC on [Ca2+]i, and also caused similar effects to those of LPC on DNA synthesis and cytotoxicity in VSMC. These observations suggest that LPC causes both cell growth and cell injury of VSMC, at least partly, through its detergent action, causing membrane leakiness and resultant [Ca2+]i overload in vitro, thus indicating the possible participation of LPC in atherosclerosis and/or injury of the vascular wall.

Animals↗
PubMed1990

The use of tetramethylbenzidine for solid phase immunoassays.

A rapid, sensitive, solid-phase immunoassay, using horseradish peroxidase and 3,3',5,5'-tetramethylbenzidine, was found to be more sensitive and the colour developed was more stable compared with HRPO using 4-chloro-1-naphthol or diaminobenzidine. Assay sensitivity was equal to or greater than that obtained with the alkaline phosphatase reaction. The essential step was to incubate filters in 1% dextran sulphate for 10 min in a pH 5 (10 mM citrate-EDTA) buffer before reacting with TMB (0.05 mg/ml in the same buffer).

Benzidines↗
PubMed1992

Quantitation of human IgG subclass antibodies to Haemophilus influenzae type b capsular polysaccharide. Results of an international collaborative study using enzyme immunoassay methodology.

An international collaborative study was conducted at ten sites to examine the performance of enzyme immunoassays (EIAs) for the quantitation of IgG1, IgG2, IgG3, IgG4 and total IgG anti-Haemophilus influenzae type b (Hib) capsular polysaccharide in human serum. All groups used the same reagents: microtiter plates coated with polyribosylribitol phosphate (PRP) conjugated to poly-L-lysine (PLL), reference, control and test human sera, biotin-conjugated International Union of Immunological Societies (IUIS)-documented monoclonal anti-human IgG1-4 and IgG Pan detection antibodies, avidin-peroxidase and TMB substrate. Initial mixing of soluble PRP antigen or an equal volume of buffer with the 20 test sera prior to analysis confirmed PRP antigen specificity in all five EIAs with greater than 80% competitive inhibition at most sites. Positive correlation between the total IgG anti-Hib and sum of IgG1-4 anti-Hib was demonstrated (r2 = 0.99, Y = 1.13X -0.15). Good agreement was shown between the total IgG anti-Hib as measured by EIA and the total Hib-specific antibodies measured by the current radiolabeled antigen binding assay (r2 = 0.97, Y = 4.6X -5.8). Assay parallelism was demonstrated with an average interdilutional %CV of 22% and parallel dose-response curve slopes. The interdilutional %CVs were calculated as an average per sample of the variation of microgram/ml (corrected for dilution) at different dilutions per laboratory for all participating sites. The interlaboratory variation was the only performance parameter studied that exceeded the target level of 35% CV in all IgG1-4 and total IgG anti-Hib assays. IgG subclass distributions in the test sera demonstrated a predominance of IgG1 anti-Hib in the pediatric serum pools and IgG2 anti-Hib in the adult sera, with low but detectable levels of IgG3 and IgG4 anti-Hib in each group.

Adult↗
PubMed1993

A rapid biochemical method for measuring antigen-induced pulmonary eosinophil margination in allergic guinea pigs.

The ability of purified guinea pig peritoneal eosinophils (EOS) to oxidise 3,3',5,5'-tetramethylbenzidine (TMB) was assessed in the presence/absence of Br- (3 mM), and compared with that of unpurified elicited peritoneal polymorphonuclear leukocytes (PMN). Br- selectively stimulated EOS peroxidase activity in a cell number-dependent manner, which was not significantly affected by the presence of diluted lung homogenate. By comparison with the peroxidase activity of added purified EOS, lung parenchyma homogenate from naive guinea pigs was estimated to contain 1.04 +/- 0.18 x 10(5) cells/mg wet tissue (n = 6), a value comparable to those calculated from published histological analyses. This was not significantly increased by ovalbumin (OA) allergen inhalation in unsensitised guinea pigs (1.4 x 10(5) EOS/mg), but was increased two-fold over the latter control to 3.0 +/- 0.18 x 10(5) cells/mg after 17 h in animals sensitised by a single injection of OA and subsequently exposed to an aerosol of bronchoactive allergen (n = 13, p < 0.05). Similar results were obtained in a parallel study using bronchoalveolar lavage (saline challenge, 20.2 +/- 2.2% EOS in lavage fluid; OA challenge, 47.1 +/- 3.6% EOS; n = 6, p < 0.05). In animals that had been doubly sensitised (two injections) to OA, the pulmonary eosinophilic response measured biochemically was more pronounced (4.9 +/- 0.2 x 10(5) cells/mg) and was significantly greater than both a non-specific protein inhalation in this sensitisation group, and OA inhalation in singly sensitised animals (n = 12, p < 0.05). Sera from the latter group was shown to contain five times less specific anti-OA IgG than the doubly sensitised animals, suggesting that EOS margination in guinea pigs is proportionate to the animals' immune status for a defined immunological challenge. These data demonstrate that in vivo EOS migration into the whole guinea pig lung can be rapidly determined by biochemical methods, and thus facilitate the in vivo assessment of novel therapeutic agents against the eosinophilic inflammation characteristic of human allergic asthma.

Animals↗
PubMed1996

Application of xanthine oxidase-catalyzed luminol chemiluminescence in a mouse interleukin-5 immunoassay.

A chemiluminescent substrate reagent for use in a sandwich immunoassay for the model antigen mouse interleukin-5 (IL-5) was developed using xanthine oxidase and luminol. Various parameters involved in this chemiluminescent reaction have been studied, including the substrate hypoxanthine, luminol and the Fe(II)-EDTA complex. Addition of the Fe(II)-EDTA complex enhances the chemiluminescence signal considerably. The xanthine oxidase-catalyzed chemiluminescent immunoassay was compared to horseradish peroxidase-linked immunoassays with luminol as chemiluminescent, and tetramethyl benzidine as colorimetric substrate. The detection limit of the xanthine oxidase-luminol assay was found to be about 0.6 pg/ml IL-5, whereas the peroxidase-catalyzed immunoassays have detection limits of about 1.3 (HRP-TMB) and 2.9 pg/ml (HRP-luminol) IL-5.

Animals↗
PubMed1996

Brain aging in normal Egyptians: neuropsychological, electrophysiological and cranial tomographic assessment.

Eighty-eight normal Egyptian volunteers above the age of 40 years were studied for brain aging and subjected to neuropsychological (the Paced Auditory Serial Addition Test; the Trailmaking test A, B; the Digit Symbol Substitution Test; sensory and secondary memory tests), electrophysiological (computerized EEG, P300 and reaction time measures), and Computerized Cranial Tomography (CCT) assessment. A significant correlation was found between age and both perception (Digit Symbol Substitution Test (DDST) and psychomotor performance (Trailmaking B test (TMb)), reaction time (RT) and the size of the third ventricle. Whereas females were worse in attention (Paced Auditory Serial Addition Test (PASAT)), males had worse performance in secondary memory test. Elderly subjects with vascular risk factors did worse in psychomotor performance (TMa) than subjects with no risk factors. Non-educated subjects showed worse perception (DSST) than educated subjects. A significant decrease in upper and lower limit percent power of the alpha band was found in subjects above 60 years, males, and non-educated subjects. A significant increase in theta activity was found only in non-educated subjects. It is concluded that decline in specific cognitive functions occurs with advancing age. Vascular risk factors and lack of education early in life enhance these changes. Moreover, the EEG slowing in the elderly was linked to lack of education early in life.

Adult↗
PubMed1982

Regulation of mast cell histamine release by neurotensin.

Neurotensin (NT), a neuropeptide found both centrally and peripherally, stimulated release of histamine from rat peritoneal mast cells in a dose-dependent manner. Release was evident by 10 nM and reached a plateau of 15-20% total cellular histamine by 10(-7)-10(-6) M NT. Optimal conditions for stimulation occurred at pH 6.5-7.5, 37 degrees C and at calcium concentrations of less than 1 mM. Release was complete within 2 minutes of peptide addition. Studies of histamine release by NT analogues indicted that the C-terminus is the biologically active portion of the molecule in this system, as is true of all other systems responsive to NT (1). D-Trp11-NT, which acts as a NT antagonist in several peripheral NT-sensitive tissues (2,3), also inhibited NT action on mast cells. Manipulations involving Ca2+ availability suggest that the mechanism of NT stimulation may involve use of intracellular Ca2+ to a greater extent than extracellular Ca2+. Lowering the extracellular Ca2+ concentration or blocking influx of extracellular Ca2+ with lanthanum (La3+), had little effect on NT-induced release, whereas Ca2+ depletion by treatment with ethylenediaminetetracetic acid (EDTA) or blockade of intracellular Ca2+ mobilization by N,N-(diethylamino)octyl 3,4,5-trimethoxybenzoate (TMB-8), inhibited the response to NT. Increasing cellular levels of adenosine 3',5'-cyclic monophosphate (cAMP), by treatment with 8-bromo-cAMP or stimulation with prostaglandin E2 (PGE2) in the presence of isobutylmethylxanthine (IBMX), served to reduce histamine release by NT, indicating that cAMP may play a role in NT stimulation.

Animals↗
PubMed1983

Effects of angiotensin II and dibutyryl cyclic adenosine monophosphate on phosphatidylinositol metabolism, 45Ca2+ fluxes, and aldosterone synthesis in bovine adrenal glomerulosa cells.

Angiotensin II (AII) and N6,O2'-dibutyryladenosine 3':5'-cyclic monophosphate (dibutyryl cyclic AMP) both stimulated aldosterone synthesis in bovine adrenal glomerulosa cells. AII altered 45Ca2+ fluxes and increased 32PO4 incorporation into phosphatidylinositol in these cells, whereas dibutyryl cyclic AMP did not affect either process. Neither AII nor dibutyryl cyclic AMP increased the mass of phosphatidylinositol. Both agents are known to stimulate pregnenolone synthesis. Thus, although dibutyryl cyclic AMP and AII may increase aldosterone synthesis at a common site (pregnenolone synthesis), they do so by different mechanisms. AII stimulation of phosphatidylinositol labeling by 32PO4 (the "PI effect") was blocked when cells were incubated in a medium containing both EGTA and the calcium antagonist, 8-(N,N-diethylamino)-octyl 3,4,5-trimethoxy-benzoate hydrochloride (TMB-8), suggesting a calcium requirement for the PI effect.

Adrenal Glands↗
PubMed1983

A calcium antagonist drug binding site in skeletal muscle sarcoplasmic reticulum: evidence for a calcium channel.

The sarcoplasmic reticulum (S.R.) of rabbit skeletal muscle has been found to contain a single, high affinity binding site for the Ca antagonist drug [3H]-nitrendipine. Two subfractions of the reticulum were studied, the heavy (HSR) and light (LSR) preparations, which exhibited similar nitrendipine equilibrium dissociation constants (KD) of 1nM. Crude cardiac and brain membranes assayed under the same conditions exhibited KD values of 0.2-0.3nM. The concentration of binding sites per mg. protein (Bmax) in HSR was found to be very high, namely 6.7 picomoles/mg, some four times greater than that of LSR. [3H]-nitrendipine binding to HSR was reversible and inhibited by the Ca antagonists flunarizine and verapamil, and by the intracellular Ca release antagonist TMB-8 (8-diethylamino-octyl 3,4,5-trimethylbenzoate hydrochloride). However, unlabelled nitrendipine at 2 X 10(-5)M had no effect on contraction of isolated electrically stimulated rabbit lumbrical or rat diaphragm muscles, nor did it affect the neuromuscular junction as studied in rat phrenic nerve-diaphragm preparations. Also, little effect of 2 X 10(-5)M nitrendipine was seen on net 45Ca uptake by HSR. These results suggest that [3H]-nitrendipine binding to skeletal muscle S.R. resembles that of brain membranes, which also contain a high affinity binding site for [3H]-nitrendipine and which similarly are pharmacologically insensitive to this dihydropyridine type of Ca channel blocking agent. Since HSR is also enriched in calsequestrin and terminal cysternae from which Ca is released in vivo, it seems likely that the [3H]-nitrendipine binding sites in S.R. are associated with Ca channels in the S.R.

Animals↗
PubMed1986

Effect of atriopeptin III on renin release in vitro.

The ability of atriopeptin III (AP) to directly inhibit renal renin release has not been resolved. This issue was examined in a series of experiments performed in a system of rat renal cortical slices (dry weight 1.91 mg) in which the goal was to explore the effects of AP on renin release induced by cyclic AMP (cAMP)-coupled stimuli or by agents which are believed to decrease intracellular calcium (Cai). Concentration response relationships were initially established for all test agents. The cAMP stimuli utilized were isoproterenol (10(-5) M), forskolin (10(-5) M), and dibutyryl cAMP (3 X 10(-4) M); each of these agents produced a significant increase in renin release in the system (with isoproterenol a 59% increase, with forskolin 37%, and with dibutyryl cAMP 52%). The addition of AP (2.09 X 10(-8) M, a minimum inhibitory concentration derived from preliminary studies) significantly blunted these increases; in the case of the dibutyryl cAMP-stimulated renin release, the inhibition was partial as a significant 25% increase in renin occurred in the presence of AP. The addition of the calcium channel blocking agent diltiazem (10(-4) M) resulted in a significant increase in renin release (364 to 567 ng X mg-1, p less than .05) which was not blocked by the addition of AP. Similarly, TMB-8 (0.6 X 10(-4) M), another agent thought to lower Cai, also resulted in increased renin release (455 to 810 ng X mg-1), p less than .01) which was also unaffected by the addition of the AP. In summary, these results show that AP is capable of partially inhibiting renin release in vitro, particularly renin release coupled to cAMP action. In contrast, renin release induced by a decline in Cai appears to be unaffected by the addition of AP.

Animals↗
PubMed1987

Effect of inhibition of Na+-K+ ATPase on the prostacyclin generation of cultured human vascular endothelial cells.

Prostacyclin (PGI2) generation of cultured human vascular endothelial cells (VEC) was observed coincidentally with the increase of 45Ca net influx. Ca ionophore A23187 enhanced not only PGI2 generation and 45Ca net influx but also 45Ca efflux. PGI2 generation was completely abolished by the pretreatment with Ca++ immobilizer, TMB-8. A Na+-K+ ATPase inhibitor, ouabain increased 45Ca net influx, but decreased 45Ca efflux, and enhanced PGI2 generation. These observation indicate that PGI2 generation of VEC may be regulated by not only Ca++ but also Na+, and it was suggested that enhanced PGI2 generation by ouabain might be derived from the increased cytosolic Ca++concentration by the decreased Ca++ efflux, and it was considered to be originated from the suppression of Na+-Ca++ exchange systems by the increased intracellular Na+ concentration via inhibition of Na+-K+ ATPase activity by ouabain. Enhancement of PGI2 generation of VEC by the increased ouabain like substances (OLS) in hypertension is suspected to be beneficial on the maintenance of vascular homeostasis.

Calcimycin↗
PubMed1993

Inhibitors of Ca2+ channels, calmodulin and protein kinases prevent A23187 and other inductions of metallothionein mRNA in EC3 rat hepatoma cells.

The role of calcium in the induction of MT mRNA has been studied in EC3 rat hepatoma cells, using various inducers (A23187, TPA, norepinephrine, and 2-chloroadenosine) and inhibitors (H7:PK-A and PK-C; W7:calmodulin; verapamil:calcium channel blocker; and TMB-8; cytosolic calcium chelator). The inhibitions of inductions observed in this study were consistent with calcium playing an important role in MT mRNA induction by itself and via crosstalk among the PK-A, PK-C, and calmodulin-dependent protein kinase pathways. Calcium has an important role in the complicated second messenger pathways which result in the positive interaction of transcription factors with the promoters of MT genes.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1996

Cellular mechanism of angiotensin II-induced atrial natriuretic peptide release in rat right atrial tissue.

This study presents an investigation of the mechanism of angiotensin II (Ang II)-induced atrial natriuretic peptide (ANP) release in superfused sliced right atria of rats. Ang II (0.1 microM) enhanced ANP release by 49%. This phenomenon was significantly blocked by (Sara1-Ileu 8) Ang II (1 microM) and losartan (0.1 microM). The use of neomycin (100 microM), a phospholipase-C inhibitor completely suppressed the effect of Ang II on ANP increase. To elucidate the intracellular mechanism of ANP released by Ang II, the role of protein kinase C (PKC) was determined by 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7) and phorbol ester : 4-beta-phorbol 12-myristate-13-acetate (PMA). We observed that PMA (0.1 microM) stimulated ANP release whereas H-7 (10 microM), an inhibitor of PKC in the presence of Ang II, prevented ANP increase. The role of calcium was also evaluated with 8-(N-N-diethylamino)-ocytyl-3,4,5, trimethoxy-benzoate (TMB-8) (10 microM) and N-(6-aminohexyl)-5-chloro-1-naphtalene sulfonamide (W-7) (10 microM), which completely inhibited ANP release by Ang II. Pre-treatment with diltiazem (10 microM), an antagonist of the Ca++ channel, did not prevent ANP increase due to Ang II, but A23187 (5 microM) enhanced ANP release by Ang II. These results suggest that PKC and intracellular calcium play an important role in ANP release under the influence of Ang II in rat atrial tissue.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1996

Serotonin-induced changes in L-leucine transport across rabbit jejunum.

The aim of the present study has been to determine the effect of serotonin (5-HT) on the absorption of L-leucine across the rabbit jejunum. The results show that serotonin significantly diminishes the uptake and steady-state tissue accumulation and the mucosal to serosal flux of L-leucine. This effect does not change with previous intestinal exposure of the mucosa to the 5-HT. Serotonin does not seem to modify amino acid simple diffusion across the intestinal epithelium. The effect on the amino acid uptake is due to an inhibition of the Na(+)-dependent system of transport, mainly through a reduction of the apparent Vmax. Moreover, this hormone, added to the incubation solution, does not affect the L-leucine uptake across brush border membrane vesicles. In presence of trifluoroperazine, TMB-8 and staurosporine, the serotonin effect disappears. These results suggest an effect mediated by intracellular processes related to protein kinase C which inhibit the intestinal absorption of L-leucine.

Animals↗
PubMed1990

Different mechanisms of increased proteolysis in atrophy induced by denervation or unweighting of rat soleus muscle.

Mechanisms of accelerated proteolysis were compared in denervated and unweighted (by tail-cast suspension) soleus muscles. In vitro and in vivo proteolysis were more rapid and lysosomal latency was lower in denervated than in unweighted muscle. In vitro, lysosomotropic agents (eg, chloroquine, methylamine) did not lessen the increase in proteolysis caused by unweighting, but abolished the difference in proteolysis between denervated and unweighted muscle. Leucine methylester, an indicator of lysosome fragility, lowered latency more in denervated than in unweighted muscle. 3-Methyladenine, which inhibits phagosome formation, increased latency similarly in all muscles tested. Mersalyl, a thiol protease inhibitor, and 8-(diethylamino)octyl-3,4,5-trimethoxybenzoate hydrochloride (TMB-8), which antagonizes sarcoplasmic reticulum release of Ca2+, reduced accelerated proteolysis caused by unweighting without diminishing the faster proteolysis due to denervation. Calcium ionophore (A23187) increased proteolysis more so in unweighted than control muscles whether or not Ca2+ was present. Different mechanisms of accelerated proteolysis were studied further by treating muscles in vivo for 24 hours with chloroquine or mersalyl. Chloroquine diminished atrophy of the denervated but not the unweighted muscle, whereas mersalyl prevented atrophy of the unweighted but not of the denervated muscle, both by inhibiting in vivo proteolysis. These results suggest that (1) atrophy of denervated, but not of unweighted, soleus muscle involves increased lysosomal proteolysis, possibly caused by greater permeability of the lysosome, and (2) cytosolic proteolysis is important in unweighting atrophy, involving some role of Ca2(+)-dependent proteolysis and/or thiol proteases.

Animals↗
PubMed1990

Contraction induced by Clostridium perfringens alpha toxin in the isolated rat ileum.

Clostridium perfringens alpha toxin caused contraction of the isolated rat ileum in a dose-dependent manner. The contraction caused by the toxin was inhibited by verapamil, nifedipine, cinnarizine, but not by tetrodotoxin or incubation in a low Na+ medium. The toxin stimulated Ca2+ uptake in the ileum in a dose-dependent manner. Nifedipine completely inhibited the Ca2+ uptake into the ileum induced by the toxin. Furthermore, TMB-8, trifluoperazine, W-7 and H-7 significantly blocked the toxin-induced contraction. On the other hand, the toxin activated de novo production of phosphatidic acid and phosphatidylinositol in the tissue. These data suggest that the toxin-induced contraction is due to an increased Ca2+ permeability across the tissue, and activation of phospholipid metabolism.

Animals↗