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Query: UMLS:C0043167 (pertussis)
 19,595 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The actions of angiotensin II (AngII) and noradrenaline (NA) on smooth muscle cells of the canine mesenteric artery were studied by measurement of isometric contractions recorded from muscle strips and the intracellular Ca2+ concentration monitored with quin2-fluorescence from dispersed suspensions of single cells. The Ca2+ transients provoked by the two agonists were monophasic in shape, i.e., after application of each agonist, [Ca2+]i rose immediately within 1 s and decreased to near-basal level within 5 min. The contraction induced by NA was maintained for several minutes whilst that induced by AngII was short-lasting. When NA was repetitively applied to the strip in Ca2+ -containing solution, the same amplitude of contractions was always obtained. In contrast, after initial exposure to AngII, subsequently-applied AngII generated small contractions. In Ca2+-free solution, either agonist could induce the large contraction. After initial exposure to NA or AngII in Ca2+ -free solution, subsequently-induced contractions by either agonist were reduced. The response induced by AngII was blocked by [Sar1, Ile8]-AngII and that of NA was blocked by phentolamine. Pertussis toxin inhibited contractions induced by both agonists but not those induced by caffeine and high K+. An activator of protein kinase C, 12-O-tetradecanoylphorbol 13-acetate (TPA), produced a slowly-developing contraction without any change in [Ca2+]i, and this agent inhibited the contractions and Ca2+ transients induced by both agonists. These results indicate that NA and AngII each act on a specific receptor and release Ca2+ from common intracellular storage sites through production of inositol 1,4,5-trisphosphate (InsP3).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Actions of angiotensin II and noradrenaline on smooth muscle cells of the canine mesenteric artery. 368 2

Variations in intracellular free calcium concentration (delta[Ca2+]i) were measured in intact and isolated human astrocytoma cells (U373 MG) loaded with fura-2 acetoxymethylester. Microperfusion of 50 nM substance P (SP), applied for 1 s, increased [Ca2+]i by 351 nM from a stable basal level of [Ca2+]i of 26 nM. The peak delta[Ca2+]i induced by SP was dose dependent with a threshold of 10(-3) nM, an ED50 of 1.3 nM and a maximal effect for concentrations of SP greater than 100 nM. The NK1 receptor agonist, [Sar9Met(O2)11]SP, mimicked the effect of SP, while the NK2 and NK3 selective receptor agonists, [N1(10)]NKA(4-10) and senktide, respectively, had no effect. The delta[Ca2+]i induced by SP was unaffected by 100 microM cadmium or by removal of extracellular calcium ions. Caffeine up to 30 mM had no effect on [Ca2+]i. In contrast, thapsigargin increased resting [Ca2+]i by 92 nM and reduced the delta[Ca2+]i induced by SP. A pertussis treatment (500 ng/ml-24 h) did not modify the delta[Ca2+]i induced by SP. We conclude that SP, acting on a NK1 receptor, mobilizes cytosolic calcium from an intracellular calcium pool which can be partially depleted by thapsigargin.
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PMID:Mobilization of intracellular calcium by substance P in a human astrocytoma cell line (U-373 MG). 752 79

The effects of platelet-activating factor (PAF) on catecholamine (CA) release and intracellular free Ca2+ concentration ([Ca2+]i) were studied in cultured bovine adrenal chromaffin cells. PAF (1 nM-1 micron) alone had no effect on [Ca2+]i and basal CA release, but potentiated the [Ca2+]i rise and CA release evoked by acetylcholine (ACh) and by elevated extracellular K+. PAF did not potentiate the responses to caffeine in Ca(2+)-deficient medium or to Bay K 8644. In chromaffin cells pretreated with either BN 50739, tetrodotoxin and amiloride or in Na(+)-deficient medium, PAF failed to potentiate the stimulation-evoked [Ca2+]i rise and CA release. In contrast, neomycin, U 73122, 5-(N-ethyl-N-isopropyl)amiloride or pertussis toxin were ineffective in blocking the potentiating effect of PAF. In a membrane fraction prepared from fresh bovine adrenal medulla, ligand-binding studies using [3H]WEB 2086 identified a PAF-displaceable binding site. These results are consistent with a model in which PAF modulates CA release by activating plasma membrane receptors that can enhance the [Ca2+]i rise via an Na(+)-dependent mechanism.
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PMID:Platelet-activating factor mediated potentiation of stimulation-evoked catecholamine release and the rise in intracellular free Ca2+ concentration in adrenal chromaffin cells. 755 78

The change of cytosolic Ca2+ concentration ([Ca2+]i) caused by vasopressin was examined in indo-1-loaded A7r5 smooth muscle cells by use of the high-performance laser cytometer and ratiometric fluorescence method. Vasopressin (100 nM) caused an initial rapid rise and a delayed increase in [Ca2+]i (n = 6). However, in the presence of tetraethylammonium chloride (10 mM), vasopressin consistently triggered sustained Ca2+ oscillations which were preceded by a large peak of [Ca2+]i. The latency for the development of this huge increase in [Ca2+]i prior to the occurrence of sustained Ca2+ oscillations was always the same. The frequency and amplitude of this type of Ca2+ oscillation varied depending upon the extracellular Ca2+ concentration. Ca(2+)-free solution did not completely suppress the sustained Ca2+ oscillations, but caffeine (20 mM) effectively abolished them. The present findings indicate that in A7r5 smooth muscle cells, the sustained Ca2+ oscillations triggered by vasopressin in the presence of tetraethylammonium chloride were mainly due to Ca2+ release from IP3-sensitive Ca2+ stores and Ca2+ influx from extracellular space, and did not require the pacemaker activity derived from the surface membrane. Moreover, the vasopressin-induced change in [Ca2+]i appeared to be linked to pertussis toxin-insensitive GTP-binding protein(s).
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PMID:Induction of Ca2+ oscillations by vasopressin in the presence of tetraethylammonium chloride in cultured vascular smooth muscle cells. 760 17

Adenosine receptors and the signaling pathways to which they are coupled were examined in dispersed intestinal muscle cells. The receptors were characterized by their ability to induce contraction or relaxation, mobilize Ca2+ and stimulate or inhibit cAMP, in naive cells and in cells where only one receptor type was preserved by selective receptor protection. Adenosine elicited contraction and increased [Ca2+]i and cAMP; the contraction was mimicked by the A1 selective agonist, cyclopentyladenosine. A selective A1 antagonist, 8-cyclopentyl-1,3-dipropylxanthine, and pertussis toxin abolished contraction and the increase in [Ca2+]i and augmented the increase in cAMP. Conversely, a preferential A2 antagonist, 9-chloro-2-(2-furyl) [1,2,4]triazolo[1,5-c]quinazolin-5-amine augmented contraction and the increase in [Ca2+]i and abolished the increase in cAMP; a cAMP-kinase inhibitor, Rp-cAMP[S], had a similar effect, augmenting contraction and the increase in [Ca2+]i. Adenosine elicited also relaxation of maximally contracted cells that increased or decreased in parallel with cAMP. The selective A2a agonist, 2-p-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamido adenosine, was a very weak relaxant agent, and the selective A2a antagonist, 8-(3-chlorostyryl)caffeine, had no effect on adenosine-induced relaxation. In cells where only A1 receptors were preserved, the cAMP response to adenosine was abolished, although contraction and [Ca2+]i were increased to the same extent as when naive cells were treated with the A2 antagonist. Conversely, in cells where only A2 receptors were preserved, contraction and the increase in [Ca2+]i were abolished and the increase in cAMP was augmented to the same level as when naive cells were treated with the A1 antagonist.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adenosine A1 and A2b receptors coupled to distinct interactive signaling pathways in intestinal muscle cells. 761 13

The effect of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX) on the voltage-dependent calcium current was studied in the clonal pituitary cell line GH3 by whole-cell patch-clamp techniques. It was found that IBMX reversibly inhibited the sustained calcium current (Ki, 1.25 mM), whereas there was no effect on the transient current. IBMX increased the inactivation rate of the sustained current without altering the voltage of activation. Vasoactive intestinal peptide, an agent known to increase cAMP, was without effect on the calcium current. The effect of IBMX was not altered by pretreating the cells with pertussis toxin or by including either cAMP or protein kinase inhibitor in the intracellular solution. The order of potency for several xanthine derivatives was IBMX > theophylline > caffeine > xanthine. The effect of IBMX on calcium current was also observed in three additional neuronal and endocrine cell lines (PC12, SY5Y, and RINm5f). These results indicate that IBMX inhibits sustained voltage-dependent calcium current by a mechanism independent of alterations in cAMP levels.
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PMID:3-Isobutyl-1-methylxanthine inhibits sustained calcium current independently of cyclic AMP in neuronal and endocrine cells. 769 Apr 52

Calcium signaling within astrocytes in the CNS may play a role comparable to that of electrical signaling within neurons. ATP is a molecule known to produce Ca2+ responses in astrocytes, and has been implicated as a mediator of intercellular Ca2+ signaling in other types of nonexcitable cells. We characterized the signal transduction pathway for ATP-evoked Ca2+ responses in cultured astrocytes from the dorsal spinal cord. Nearly 100% of these astrocytes respond to extracellularly applied ATP, which causes release of Ca2+ from an intracellular pool that is sensitive to thapsigargin and insensitive to caffeine. We found that intracellular administration of IP3 also caused release of Ca2+ from a thapsigargin-sensitive intracellular pool, and that IP3 abolished the response to ATP. The ATP-evoked Ca2+ response was blocked by the IP3 receptor antagonist heparin, applied intracellularly, but not by N-desulfated heparin, which is not an antagonist at these receptors. The Ca2+ response caused by ATP was also blocked by a phospholipase C inhibitor, U-73122, but not by its inactive analog, U-73343. Increases in [Ca2+]i were elicited by intracellular application of activators of heterotrimeric G-proteins, GTP gamma S and AIF4-. On the other hand, [Ca2+], was unaffected by a G-protein inhibitor, GDP beta S, but it did abolish the Ca2+ response to ATP. Pretreating the cultures with pertussis toxin did not affect responses to ATP. Our results indicate that in astrocytes ATP-evoked release of intracellular Ca2+ is mediated by IP3 produced as a result of activating phospholipase C coupled to ATP receptors via a G-protein that is insensitive to pertussis toxin. ATP is known to be released under physiological and pathological circumstances, and therefore signaling via the PLC-IP3 pathway in astrocytes is a potentially important mechanism by which ATP may play a role in CNS function.
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PMID:ATP causes release of intracellular Ca2+ via the phospholipase C beta/IP3 pathway in astrocytes from the dorsal spinal cord. 772 40

We have examined the effects of the muscarinic agonists, carbachol (CCh) and oxotremorine (Oxo), on the intracellular free Ca2+ concentration ([Ca2+]i) in acutely dissociated sympathetic neurons from adult rats using fura 2-based microfluorometry. The drugs increased [Ca2+]i by 86 +/- 7 and 38 +/- 10 nM for CCh and Oxo, respectively (both 10 microM). Basal [Ca2+]i was 52 +/- 3 nM. Depletion of the caffeine-sensitive Ca2+ store or blockade of the Ca(2+)-adenosinetriphosphatase with thapsigargin did not alter the effect of either agonist on the rise in [Ca2+]i. On the other hand, the omission of Ca2+ from the perfusion solution or the use of TA-3090, a Ca2+ channel antagonist, blocked the effects of CCh and Oxo. In whole cell current-clamp recordings, the muscarinic agonists elicited a depolarization and action potential firing, which probably explained the rise in [Ca2+]i observed with microfluorimetric recording. In addition to their direct effects on the [Ca2+]i, muscarinic agonists also reduced the rise in [Ca2+]i induced by a nicotinic agonist. This inhibitory effect, observed in 68% of cells that responded to the nicotinic agonist, was blocked by atropine and pertussis toxin, whereas the muscarinic agonist-induced increase in [Ca2+]i was blocked by atropine but was pertussis toxin insensitive. These results suggest that at least two muscarinic receptors are present on sympathetic neurons and that they mediate opposite effect on the fluctuation of [Ca2+]i.
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PMID:Increase in [Ca2+]i by CCh in adult rat sympathetic neurons are not dependent on intracellular Ca2+ pools. 773 31

Intracellular free Ca2+ concentrations ([Ca2+]i) were measured in subclones of NL308 neuroblastoma x fibroblast hybrid cells expressing each of the individual muscarinic acetylcholine receptor (mAChR) subtypes m1, m2, m3 and m4. Application of 100 microM acetylcholine (ACh) increased [Ca2+]i in all four subclones. The increased [Ca2+]i levels were significantly higher in m1- and m3-transformed cells than those in m2- and m4-transformed cells. In more than 95% of m2- and m4-transformed cells, [Ca2+]i showed sinusoidal oscillations. ACh-induced increases in [Ca2+]i were not observed in cells treated with an intracellular Ca2+ chelator, 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA). Removal of extracellular Ca2+ with ethylene-glycol-bis-(beta- aminoethyl)-N,N,N',N'-tetraacetate (EGTA) did not affect the initial [Ca2+]i increases, but reduced the late phases of delta [Ca2+]i in ml- and m3-transformed cells by 20-30%. Oscillations in m2- and m4-transformed cells persisted in EGTA solution (though sometimes slowed in frequency), suggesting that they were of intracellular origin. ACh-induced delta [Ca2+]i and inositol 1,4,5-trisphosphate formation was completely suppressed by pre-treatment with 50-100 ng ml-1 Pertussis toxin (PTX) for 12 h in m2- and m4-transformed cells, but not in m1- and m3-transformed cells. In all cells, extracellular application of caffeine and ryanodine, or intracellular application of cyclic adenosine diphosphate ribose (cAD-PR) produced a rise in [Ca2+]i. ACh-induced [Ca2+]i oscillations were not observed in ryanodine-treated m2-transformed cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inositol 1,4,5-trisphosphate formation and ryanodine-sensitive oscillations of cytosolic free Ca2+ concentrations in neuroblastoma x fibroblast hybrid NL308 cells expressing m2 and m4 muscarinic acetylcholine receptor subtypes. 776 Dec 66

Adenosine exerts pronounced biological effects in the heart cell. The role of multiple adenosine receptor subtypes in regulating the heart cell function is not known. Ventricular cells cultured from chick embryos 14 days in ovo were used to study a novel feature of heart cell regulation by the stimulatory adenosine receptors. The inhibitory adenosine A1 receptor pathway was first inactivated by pertussis toxin treatment of the cultures, and the effects of adenosine agonists and antagonists on the heart cell contractile amplitude, measured via an opticovideo motion detection system, and on the modulation of cAMP level were determined. Adenosine and N-ethyladenosine-5'-uronic acid (NECA), capable of activating both the adenosine A2a and A2b receptors, caused a greater increase in the contractile amplitude than did the A2a-selective agonist 2-[4-(2-carboxythyl)phenylethylamino]-5'-N-ethylcarboxamidoa denosine (CGS21680). NECA caused a biphasic increase in cAMP, which became monophasic in the presence of the A2a receptor-selective antagonist 8-(3-chlorostyryl)caffeine, whereas the CGS21680-induced cAMP response was monophasic. Blocking with 8-(3-chlorostyryl)caffeine abolished most of the CGS21680-elicited contractile or cAMP response while attenuating only part of the adenosine- or NECA-stimulated responses. Blocking with the A2b-selective antagonists 1,3-diethyl-8-phenylxanthine or alloxazine caused a more pronounced inhibititon of the contractile or cAMP response by adenosine or NECA than by CGS21680. Affinity of the A2a receptor was 60-fold higher than that of the A2b receptor. These data demonstrate that a functional A2b receptor is expressed on the heart cell and is capable of mediating augmentation of cardiac myocyte contractility and that adenosine A2a and A2b receptors, with greatly different affinity, coexist and are coupled to the same functional responses. Taken together, the data suggest a novel feature of heart cell regulation, where the high-affinity A2a receptor can play an important modulatory role in the presence of a low level of adenosine, whereas the low-affinity A2b receptor becomes functionally important when the adenosine level is high.
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PMID:Adenosine A2a and A2b receptors in cultured fetal chick heart cells. High- and low-affinity coupling to stimulation of myocyte contractility and cAMP accumulation. 783 35


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